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Diabetes, insulin resistance and sugars
Abstract
Insulin resistance is associated with type 2 diabetes, hypertension and cardiovascular disease and the dietary factors involved in these metabolic disorders are still misunderstood. In animal studies, sugars, particularly sucrose and fructose, have been shown to decrease insulin sensitivity, with potential association with an induced hypertriglyceridemia. But in humans, the effects of sugars on insulin sensitivity are still debated.
The present work first gives an overview of the metabolic pathways that could be implicated in the development of insulin resistance by sugars. Then, a review of the studies (intervention, prospective and cross‐sectional) on the relationship between sugars, insulin resistance and diabetes is made in order to determine the level of proof concerning the association of sugars consumption and diabetes.
All these studies failed to demonstrate an obvious relationship between the intake of total simple carbohydrates and glycaemic control or risk to develop a type 2 diabetes and particularly specific evidence is missing in terms of sucrose effect on diabetes.
Concerning fructose, there are still discrepancies between studies' conclusions about the long‐term deleterious effect on diabetes development. But its effect on lipogenesis and triglyceridemia has to be taken into account, considering the growing use of fructose in food industry and sugar‐sweetened drinks.
... T1DM is an autoimmune disease leads to the destruction of pancreatic β cells accounts for less than 10% of the diabetic population while the rest 90% is T2DM. Glucose homeostasis in the body is regulated by the hormone insulin, which is secreted by pancreatic β cells (4)(5)(6). Increased extracellular glucose triggers a rapid upregulation of insulin secretion from the insulin storage granules and the secreted insulin is replenished by increased insulin biosynthesis through the activation of diverse gene regulatory mechanisms (5,7,8). In early stages of the T2DM, β cells increase their mass and insulin production to maintain glucose levels and overcome insulin resistance (9,10). ...
... Glucose homeostasis in the body is regulated by the hormone insulin, which is secreted by pancreatic β cells (4)(5)(6). Increased extracellular glucose triggers a rapid upregulation of insulin secretion from the insulin storage granules and the secreted insulin is replenished by increased insulin biosynthesis through the activation of diverse gene regulatory mechanisms (5,7,8). In early stages of the T2DM, β cells increase their mass and insulin production to maintain glucose levels and overcome insulin resistance (9,10). ...
... Sucrose, glucose and fructose solutions are normally consumed as sugar in human diets. Yet, it has been shown that diets with high sucrose and high fructose can reduce insulin sensitivity in animals (5), and cause skeletal muscle insulin resistance (6). Moreover, a number of studies have indicated that high fat and high sucrose feed lower the uptake of glucose in muscles (6,7). ...
... Moreover, a number of studies have indicated that high fat and high sucrose feed lower the uptake of glucose in muscles (6,7). Likewise, consumption of foods containing high levels of simple sugars can reduce insulin sensitivity (8) and can induce diabetes (5). Herbs have been used as alternative medicines in various diseases (9). ...
Introduction: Inocutis levis is a polypore fungus belonging to Hymenochaetales of basidiomycetes. The specie is mainly distributed in Asia and grows on living angiosperm trees. This study investigates the effect of aqueous extract of I. levis on insulin resistance and glucose tolerance in high sucrose fed (HSF) rats. Methods: Male rats were given 30% sucrose solution for 12 weeks. The extract of I. levis at doses of 50 and 150 mg/kg body weight was intraperitoneally administered for 2 weeks in HSF rats. Blood glucose, serum insulin, insulin resistance index (HOMA-IR) and histological changes of pancreas were evaluated. Results: Sucrose solution significantly increased the insulin, glucose and HOMA-IR levels, compared to the control. At the dose of 50 mg/kg the extract decreased glucose and insulin, and improved insulin resistance relative to that of HSF rats which did not take the extract. Histological studies on pancreas tissue indicated no significant difference in the size of Langerhans islets of HSF rats and HSF rats treated with the extract at dose of 50 mg/kg compared to the control group. But, treatment with the dose of 150 mg/kg of I. levis increased islets diameter and number of cells in the islets of Langerhans in HSF group. Conclusion: Inocutis levis extract may have hypoglycemic effects, by regulating insulin secretion and improving glucose tolerance, and seems to be able to ameliorate pancreatic islets in HSF rats. Our findings indicate that I. levis can be considered as a potential treatment with medicinal properties to alleviate insulin resistance and to prevent risk of type 2 diabetes in a dose dependent manner.
... Adiposity is causally linked to insulin resistance, T2DM, dyslipidemia, and high BP, which are components of MetS. 211 A high intake of sugars will also increase blood glucose and insulin secretion independent of total energy intake. In this situation, insulin hypersecretion may lead to insulin resistance, T2DM, and diabetic dyslipidemia (high TGs, low HDL-C). ...
... In this situation, insulin hypersecretion may lead to insulin resistance, T2DM, and diabetic dyslipidemia (high TGs, low HDL-C). 211 Sugar-sweetened beverages (SSBs) are responsible for a large proportion of total sugar and energy intake in both developed and developing countries. 212 Sugarsweetened beverages are also unique in that they are not as satiating as solid foods, which could lead to overconsumption of energy. ...
The importance of metabolic syndrome (MetS) lies in its associated risk of cardiovascular disease and type 2 diabetes, as well as other harmful conditions such as nonalcoholic fatty liver disease. In this report, the available scientific evidence on the associations between lifestyle changes and MetS and its components is reviewed to derive recommendations for MetS prevention and management. Weight loss through an energy-restricted diet together with increased energy expenditure. © The Author(s) 2017. Published by Oxford University Press on behalf of the International Life Sciences Institute.
... Additionally, it has been hypothesized that the ASBs might stimulate appetite and increase calorie intake (Blundell and Hill, 1986;Pepino, 2015). For a long time, there has been considerable debate and conflicting opinions regarding how specific sugars affect the development of type 2 diabetes rather than excess calories per se (Qi and Tester, 2020;Laville and Nazare, 2009). In this study, we have provided new evidence indicating that the administration of noncaloric monosaccharides leads to significant excessive angiogenesis, suggesting that the excessive angiogenesis may not be only attributed to the caloric properties. ...
Artificially sweetened beverages containing noncaloric monosaccharides were suggested as healthier alternatives to sugar-sweetened beverages. Nevertheless, the potential detrimental effects of these noncaloric monosaccharides on blood vessel function remain inadequately understood. We have established a zebrafish model that exhibits significant excessive angiogenesis induced by high glucose, resembling the hyperangiogenic characteristics observed in proliferative diabetic retinopathy (PDR). Utilizing this model, we observed that glucose and noncaloric monosaccharides could induce excessive formation of blood vessels, especially intersegmental vessels (ISVs). The excessively branched vessels were observed to be formed by ectopic activation of quiescent endothelial cells (ECs) into tip cells. Single-cell transcriptomic sequencing analysis of the ECs in the embryos exposed to high glucose revealed an augmented ratio of capillary ECs, proliferating ECs, and a series of upregulated proangiogenic genes. Further analysis and experiments validated that reduced foxo1a mediated the excessive angiogenesis induced by monosaccharides via upregulating the expression of marcksl1a . This study has provided new evidence showing the negative effects of noncaloric monosaccharides on the vascular system and the underlying mechanisms.
... Moreover, the relatively low sugar content could potentially make it suitable for low-calorie diets, which are suggested for obese and diabetic patients. 54 Further studies exploring the glycemic index and cholesterol levels of this plant could provide an understanding of the blood sugar response and overall effects on the body. Nevertheless, C. latifolia fruits have promising nutritional content and can be a valuable supplement for a healthy body. ...
Curculigo latifolia Dryand. ex W. T. Aiton, from the genus Curculigo, is a medicinal plant traditionally used to treat numerous illnesses such as fever, stomach aches, jaundice, wounds, and inflammation. C. latifolia is a perennial herb that is widely found in tropical and subtropical regions, such as Southeast Asia, Southern China, Bangladesh, Australia, and the Andaman Islands. This review collates the reported studies on the different aspects of C. latifolia from its plant description, nutritional value, phytochemistry, chemical composition, and pharmacological properties. This review aims to identify gaps in the literature and provide useful references for future work on this plant. Previous studies have shown that C. latifolia contains high mineral contents of calcium, iron, and magnesium, which are essential components of human health. Moreover, the plant is rich in phytochemicals, which play a prominent role in various pharmacological activities. The most common compounds identified included curculigoside, crassifoside I, nyasicoside, and curculigine. C. latifolia demonstrated high antioxidant activity through its ability to scavenge superoxide anions, 1,1–diphenyl–2–picrylhydrazyl (DPPH) and 2,2’-azino–bis(3–ethylbenzthiazoline–6–sulfonic acid) (ABTS) radicals, reducing ferric ions to ferrous complexes, iron chelation, and β –carotene bleaching. It was also shown that the roots, stems, and leaves of C. latifolia were effective in exerting antimicrobial activity against several microbial strains, including Bacillus cereus, Bacillus subtillis, Enterobacter aerogenes, Erwinia sp. , Klebsiella sp., Pseudomonas sp., Candida albicans, Salmonella choleraesuis and Staphylococcus aureus. Moreover, the root, fruit, leaf, petiole, and rhizome extracts were found to improve glucose uptake and insulin secretion in diabetic rats, suggesting their antidiabetic potential. C. latifolia presents a wide range of medicinal properties that could make it a promising functional food or source of food supplements to prevent nutrition–related or chronic diseases.
... Moreover, the relatively low sugar content could potentially make it suitable for low-calorie diets, which are suggested for obese and diabetic patients. 54 Further studies exploring the glycemic index and cholesterol levels of this plant could provide an understanding of the blood sugar response and overall effects on the body. Nevertheless, C. latifolia fruits have promising nutritional content and can be a valuable supplement for a healthy body. ...
Curculigo latifolia Dryand. ex W. T. Aiton, from the genus Curculigo, is a medicinal plant traditionally used to treat numerous illnesses such as fever, stomach aches, jaundice, wounds, and inflammation. C. latifolia is a perennial herb that is widely found in tropical and subtropical regions, such as Southeast Asia, Southern China, Bangladesh, Australia, and the Andaman Islands. This review collates the reported studies on the different aspects of C. latifolia from its plant description, nutritional value, phytochemistry, chemical composition, and pharmacological properties. This review aims to identify gaps in the literature and provide useful references for future work on this plant. Previous studies have shown that C. latifolia contains high mineral contents of calcium, iron, and magnesium, which are essential components of human health. Moreover, the plant is rich in phytochemicals, which play a prominent role in various pharmacological activities. The most common compounds identified included curculigoside, crassifoside I, nyasicoside, and curculigine. C. latifolia demonstrated high antioxidant activity through its ability to scavenge superoxide anions, 1,1–diphenyl–2–picrylhydrazyl (DPPH) and 2,2’-azino–bis(3–ethylbenzthiazoline–6–sulfonic acid) (ABTS) radicals, reducing ferric ions to ferrous complexes, iron chelation, and B-carotene bleaching. It was also shown that the roots, stems, and leaves of C. latifolia were effective in exerting antimicrobial activity against several microbial strains, including Bacillus cereus, Bacillus subtillis, Enterobacter aerogenes, Erwinia sp. , Klebsiella sp., Pseudomonas sp., Candida albicans, Salmonella choleraesuis and Staphylococcus aureus. Moreover, the root, fruit, leaf, petiole, and rhizome extracts were found to improve glucose uptake and insulin secretion in diabetic rats, suggesting their antidiabetic potential. C. latifolia presents a wide range of medicinal properties that could make it a promising functional food or source of food supplements to prevent nutrition–related or chronic diseases.
... Lowering their glucose levels required more time and larger amounts of insulin. The assumptions to explain this are as follows: 1. Diabetic patients have adapted to chronic hyperglycemia and have resistance to lowering glucose with the same insulin dose due to insulin resistance and beta-cell secretory defects [40,41]. Especially in patients who have already been diagnosed with and treated for diabetes, despite the intervention of glucose-lowering medication, it might be expected that more effort would be required to reach the target because of their being in a state of poor glycemic control. ...
Hyperglycemia is commonly observed in critically ill patients and postcardiac arrest patients, with higher glucose levels and variability associated with poorer outcomes. In this study, we aim to compare glucose control in diabetic and nondiabetic patients using glycated hemoglobin (HbA1c) levels, providing insights for better glucose management strategies. This retrospective observational study was conducted at Seoul St. Mary’s Hospital from February 2009 to May 2022. Blood glucose levels were measured hourly for 48 h after return of spontaneous circulation (ROSC), and a glucose management protocol was followed to maintain arterial blood glucose levels between 140 and 180 mg/dL using short-acting insulin infusion. Patients were categorized into four groups based on diabetes status and glycemic control. The primary outcomes assessed were neurological outcome and mortality at 6 months after cardiac arrest. Among the 332 included patients, 83 (25.0%) had a previous diabetes diagnosis, and 114 (34.3%) had an HbA1c of 6.0% or higher. At least one hyperglycemic episode was observed in 314 patients (94.6%) and hypoglycemia was found in 63 patients (19.0%) during 48 h. After the categorization, unrecognized diabetes was noticed in 51 patients with median HbA1c of 6.3% (interquartile range [IQR] 6.1–6.6). Patients with inadequate diabetes control had the highest initial HbA1c level (7.0%, IQR 6.5–7.8) and admission glucose (314 mg/dL, IQR 257–424). Median time to target glucose in controlled diabetes was significantly shorter with the slowest glucose reducing rate. The total insulin dose required to reach the target glucose level and cumulative insulin requirement during 48 h were different among the categories (p <0.001). Poor neurological outcomes and mortality were more frequently observed in patients with diagnosed diabetes. Occurrence of a hypoglycemic episode during the 48 h after ROSC was independently associated with poor neurologic outcomes (odds ratio [OR] 3.505; 95% confidence interval [CI], 2.382–9.663). Surviving patients following cardiac arrest exhibited variations in glucose hemodynamics and outcomes according to the categories based on their preexisting diabetes status and glycemic condition. Specifically, even experiencing a single episode of hypoglycemia during the acute phase could have an influence on unfavorable neurological outcomes. While the classification did not directly affect neurological outcomes, the present results indicate the need for a customized approach to glucose control based on these categories.
... Numerous studies have reported an association between reduced salt intake and a reduced likelihood of metabolic syndrome [42,43]. This association may be attributed to the fact that high salt intake decreases the body's baseline aldosterone levels and increases the activity of the salt corticosteroid receptor, thereby contributing to metabolic disruptions [44] by interfering with insulin signaling pathways [45]. Livestock and poultry meats, salt, and added sugar are dietary components with pro-inflammatory properties that promote chronic inflammation within the body. ...
Background
This study aims to investigate the relationship between gestational metabolic syndrome (GMS) and the Chinese Healthy Eating Index (CHEI) in mid-pregnancy, and to identify potentially beneficial or high-risk dietary habits. We have developed a mid-pregnancy version of CHEI-2022, adapting the Chinese Healthy Eating Index to align with the food quantity recommendations outlined in the 2022 Dietary Guidelines for Chinese Residents for mid-pregnancy.
Methods
Using the inclusion and exclusion criteria, data from 2411 mid-pregnant individuals were collected through interviews. The Total CHEI score and its component scores were determined through analysis of responses from the food frequency questionnaire. GMS diagnosis involved conducting physical examinations and performing blood biochemical tests. A logistic regression model was employed to analyze the relationship between GMS or related indices and both the total CHEI score and its component scores.
Results
The study identified an overall GMS prevalence of 21.65% (522 out of 2411 participants). During mid-pregnancy, participants diagnosed with GMS exhibited higher BMI, FBG, 1hPBG, 2hPBG, TC, TG, HDL, SBP, as well as higher educational levels and daily activity, compared to those without GMS (P < 0.001). After adjusting for potential confounders, participants with higher total CHEI scores (≥ 80) were found to have lower odds of GMS or related indices (P < 0.05). Increasing dietary intake of potatoes, whole grains, beans, dark green vegetables, and fruits, as per the CHEI recommendations, was associated with reduced odds of GMS or related indices (P < 0.05).
Conclusion
A high-quality diet, as indicated by a total CHEI score of 80 or higher, and increased consumption of specific dietary components, namely potatoes, beans, dark green vegetables, and fruits, were found to effectively reduce the odds of GMS or related indices during mid-pregnancy.
... The inability to store excess energy in mature adipose tissue and small adipocytes' impairment in triglyceride storage processing and impaired adipogenesis have been proposed as potential mechanisms for the aforementioned association and results in more fat deposited in the liver and muscle [2,15]. Moreover, patients with type 2 diabetes, a group characterized by decreased insulin sensitivity [16], had increased fraction of small adipocytes compared with BMImatched controls without diabetes [17]. We found no change in small cell percentage despite clinically meaningful weight loss of 8-9%. ...
Objective
Adipose tissue (AT) contains a bimodal population of large and small adipocytes. Changes in fat cell size (FCS) distribution and AT caloric density (kcal/g) with weight loss are unclear. We aimed to evaluate changes in FCS and AT calories in weight loss and determine associations with anthropometrics.
Materials and methods
Healthy adults (6 men/4 women; age 33 ± 11 years; BMI 35 ± 6 kg/m²) underwent DXA and subcutaneous abdominal/thigh fat biopsies, before and after 6 weeks of caloric restriction. AT calories (bomb calorimetry) and hormones (adiponectin, leptin, FGF21) were measured.
Results
Abdominal large cell diameter (LCD; Δ = −13.2 μm, p = 0.01) and nadir (Δ = −7.3 μm, p = 0.03) decreased. In repeated measures correlations (rrm), abdominal and thigh LCD and nadir were associated with fat mass (FM) loss (rrm = 0.68; rrm = 0.63; rrm = 0.66; rrm = 0.62, p’s < 0.05, respectively) and waist circumference decrease (rrm = 0.70; rrm = 0.60, p’s ≤ 0.05). Small cell percentage did not change and was not associated with FM changes. Abdominal AT calories were unchanged with weight loss. Change in leptin was associated with change in abdominal LCD (rrm = 0.77, p = 0.01).
Conclusions
Caloric restriction reduces adipocyte LCD and nadir. These changes are associated with FM loss. Larger fat cells should be considered as phenotypic targets for weight loss.
Clinical Trials Registration
clinicaltrials.gov identifier: NCT00687115, May 29, 2008
... The risk of GMS relative indexes, including overweight/obesity, GDM, hypertension and dyslipidemia, also increased signi cantly with increased intake of livestock and poultry meats, sugar, and salt. Several previous studies have also shown that a higher intake of livestock and poultry meats can increase the prevalence of metabolic disorders [38,39].A prospective clinical observation of 2,755 cases found that meat-related dietary patterns were signi cantly associated with the prevalence of GDM [40].A prospective study of 1,868 middle-aged and older adults showed that poultry and processed meats may increase the risk of metabolic syndrome, and that substituting other proteinrich foods, such as beans, sh, and eggs for poultry meat may be effective in preventing metabolic syndrome [41].Many studies have also reported that reduced salt intake is associated with a reduced risk of metabolic syndrome [42,43], possibly because a high salt intake reduces the baseline aldosterone levels of the body and increases the activity of the salt corticosteroid receptor, leading to metabolic disturbances [44] by interfering with insulin signaling pathways [45].Livestock and poultry meat, salt, and added sugar are pro-in ammatory dietary components, which promote chronic in ammation in the body and increase levels of in ammatory indices, such as TNF-α, interleukin (IL)-1β, IL-4, IL-6, and IL-10, thus promoting IR. The pro-in ammatory diet also includes re ned carbohydrates, saturated fatty acids, and trans-fatty acids, but this study did not nd the energy supply ratio of carbohydrates and oil consumption was associated with the risk of GMS, probably because pregnant women themselves focus on nutritional health by increasing the proportion of whole grains in their staple diet, as well as using soybean oil, corn oil, and olive oil as cooking oil during pregnancy. ...
Background We established a mid-pregnancy version of CHEI-2022 based on the Chinese Healthy Eating Index (CHEI), with reference to the amount of food recommended by Dietary Guidelines for Chinese Residents (DGC-2022) for mid-pregnancy. To explore the relationship between gestational metabolic syndrome (GMS) and the CHEI in mid-pregnancy and to identify potentially beneficial or high-risk dietary habits.
Methods Based on the inclusion and exclusion criteria, the data of 2,411 mid-pregnancy was collected by interview. Total CHEI score and its component scoreswere calculated based on the food frequency questionnaire. Physical examination and blood biochemical tests were used to diagnose GMS. The logistic regression model was used to analyze the relationship between GMS or relative indexes and the total CHEI score or its component scores.
Results The study showed the overall prevalence of GMS was 21.65%(522/2,411). Mid-pregnancy with GMS had a higher BMI, FBG, 1hPBG, 2hPBG, TC, TG, HDL, SBP, degree of education, and daily activity than those without GMS (p < 0.001).After adjusting for potential confounders, it showed that the higher total CHEI scores(≥ 80) ,the lower risk of GMSor relative indexes (P<0.05). The GMS or relative indexes risks were reduced by increasing the dietary content of potatoes, whole grains, beans, dark green vegetables, and fruits in the CHEI (P < 0.05).
Conclusion The quality of healthy diet (total CHEI score≥ 80) and increased intake of specificdietary components (potatoes, beans, dark green vegetables ,fruits) were effective in reducing the risk of GMS or relative indexes in mid-pregnancy.
... There is a close relationship between NAFLD and type 2 diabetes mellitus (T2DM) [3]. Insulin resistance, obesity and dyslipidemia are the main factors in the pathogenesis of NAFLD and T2DM [4][5][6]. The worldwide prevalence of NAFLD is 25.24%, and the prevalence of T2DM in the general population is estimated to be 6.3% [7,8]. ...
Background
Patients with non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes mellitus (T2DM) are at increased risk for cardiovascular diseases (CVD). Omega-3 supplementation has been proposed as a possible strategy for management of cardiometabolic risk. Cardiometabolic indices can predict and evaluate the cardiometabolic risk.
Aims
We investigated the effect of omega-3 supplementation on accurate and available cardiometabolic indices including atherogenic index of plasma (AIP), Castelli risk index I, Castelli risk index II and atherogenic coefficient (AC) in diabetic patients with NAFLD.
Methods
We conducted a double-blind, randomized controlled trial (RCT) for 12 weeks. From August 2016 to March 2017, the subjects referred to Faghihi hospital in Shiraz, Iran, were recruited. Sixty diabetic patients with NAFLD were randomly assigned into the omega-3 (2000 mg/d omega-3 capsule contained 360 mg/d eicosapentaenoic acid and 240 mg/d docosahexaenoic acid) and the placebo (liquid paraffin) groups using computer-generated random number table.
Results
Omega-3 supplementation compared to the placebo had no significant effect on AIP (− 0.11 ± 0.20 vs. -0.03 ± 0.16; P = 0.11), Castelli risk index I (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42), Castelli risk index II (− 0.24 ± 0.5 vs. -0.14 ± 0.5; P = 0.63) and AC (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42). After adjusting for confounding factors, the findings remained without change.
Conclusion
Omega-3 supplementation (2000 mg/d) for 12 weeks has no effect on cardiometabolic risk. It seems, higher doses of omega-3 can improve cordiometabolic risk. The trial was registered at Iranian Registry of Clinical Trials IRCT2016102530489N1.
... La ingesta de este tipo de azúcares añadidos aumenta la secreción de glucosa e insulina independientemente de la ingesta total de energía A su vez, la hipersecreción de insulina favorece la resistencia a la insulina, la obesidad visceral, el síndrome metabólico y la DM2 (6,185) , así como otras condiciones asociadas, destacando el hígado graso no alcohólico (186) y la dislipidemia aterogénica (187) . Estos azúcares tienen muy poca capacidad saciante, favoreciendo su consumo de forma continuada y en muchas ocasiones fuera de los horarios de las comidas. ...
... These features have been linked with reducing of blood pressure, total cholesterol, and LDL-cholesterol levels (Dow et al., 2012). In addition, grapefruit consumption plays a role in the control of insulin levels and prevents insulin resistance and type 2 diabetes (Laville & Nazare, 2009). ...
Citrus fruits are one of the world’s most popular, easily accessible, nutritiously desirable, and healthy fruits. Citrus varieties are accepted as a rich source of mainly vitamin C, folate, tocols, fiber, and bioactive compounds such as flavonoids, carotenoids, phenolic acids, and limonoids. Lemon (Citrus limon), orange (Citrus sinensis), grapefruit (Citrus paradisi), shaddock (Citrus maxima), tangerine (Citrus reticulata), citron (Citrus medica), and key lime (Citrus aurantifolia) are commonly known popular citrus varieties belonging to the Rutaceae family. Citrus peels, seeds and pulps as by-products, which represents 50% of the raw fruit, are considered unique sources of fixed and essential oils. When considering the aroma characteristics and volatile compositions of essential oils, citrus essential oils were identified as having an important role as a flavoring agent for food, cosmetic, aromatherapy, and pharmacology. Cold pressing is a widely used technique for extraction of citrus essential oils as well as the steam distillation technique, and cold pressed citrus oils have been classified as generally recognized as safe (GRAS). Cold pressed grapefruit oils have a characteristic bitter taste and distinct aroma that can be obtained from grapefruit peel, leaves, or seeds. Due to their great distinctive and nutraceutical composition, numerous studies have indicated the biological activities of cold pressed grapefruit oils. This chapter presents the current scientific knowledge on the cold pressing technique for extraction of grapefruit oils, focusing on compositional properties, bioactive components, volatile compounds, sensory attributes, and beneficial health effects of cold pressed grapefruit oils.
... Diabetes is one of the most common diseases in the world [1]. Diabetes is characterized by increased blood glucose levels due to the dysfunctional sensing or production of insulin [2,3]. Pancreatic β-cells synthesize and secrete insulin to maintain glucose homeostasis in the body [4]. ...
Circular RNAs (circRNAs) are a large family of noncoding RNAs that have emerged as novel regulators of gene expression. However, little is known about the function of circRNAs in pancreatic β-cells. Here, transcriptomic analysis of mice pancreatic islet RNA-sequencing data identified 77 differentially expressed circRNAs between mice fed with a normal diet and a high-fat diet. Surprisingly, multiple circRNAs were derived from the intron 2 of the preproinsulin 2 (Ins2) gene and are termed as circular intronic (ci)-Ins2. The expression of ci-Ins2 transcripts in mouse pancreatic islets, and βTC6 cells were confirmed by reverse transcription PCR, DNA sequencing, and RNase R treatment experiments. The level of ci-Ins2 was altered in βTC6 cells upon exposure to elevated levels of palmitate and glucose. Computational analysis predicted the interaction of several RNA-binding proteins with ci-Ins2 and their flanking region, suggesting their role in the ci-Ins2 function or biogenesis. Additionally, bioinformatics analysis predicted the association of several microRNAs with ci-Ins2. Gene ontology and pathway analysis of genes targeted by miRNAs associated with ci-Ins2 suggested the regulation of several key biological processes. Together, our findings indicate that differential expression of circRNAs, especially ci-Ins2 transcripts, may regulate β-cell function and may play a critical role in the development of diabetes.
... In our experiments, mice were made to exercise for approximately 70-75% of maximum oxygen uptake. However, high intensity exercise can also mediate stress related hormones, such as glucocorticoids, cortisol, and catecholamine 13 that trigger the release of glucose stored as glycogen into the bloodstream, leading to high blood sugar levels, an insulin response, and therefore, metabolic diseases 46 . ...
Purpose:
The purpose of this study was to determine whether different types of carbohydrate diets with or without exercise changes energy metabolism at rest and during exercise.
Methods:
To minimize differences in food and energy intake between experimental groups, mice were pair-fed. After 1 week of adaptation, 40 male ICR mice (6 weeks old) were randomly divided into four groups: Sta. (high fat + high starch), Scu. (high fat + high sucrose), StaEX. (high fat + high starch + exercise), and SucEX. (high fat + high sucrose + exercise). StaEX. and ScuEX. groups underwent training by running on a treadmill five times a week. After 10 weeks of training, energy metabolism was measured for 24 h and during a 1 h exercise period.
Results:
The final body weight showed no significant difference between the groups. However, the weight of abdominal tissues (epididymal, perirenal, and mesenteric adipose tissue) in training groups was markedly decreased following 10 weeks of training. Results of all energy metabolism (24 h at rest and during 1 h of exercise) showed no significant interactions between diet and exercise. A brief summary of the results of the energy metabolism is that the metabolism related indicators over 24 h were more affected by the dietary pattern than the exercise but during the 1 h of exercise, training had more effect on energy metabolism than diet.
Conclusion:
Our findings confirm that: (a) the type of carbohydrates included in the diet influence the metabolic responses over 24 h, (b) training had more effect on energy metabolism than diet during 1 h of exercise, (c) both results; abdominal adipose tissue weight and fat oxidation during exercise are suggestive for a beneficial effect of moderate physical activity on weight maintenance.
... High-sucrose intake was shown to contribute syndromes such as hyperlipidemia, glucose intolerance, hypertension, and cardiovascular complications (5). A diet too rich in sucrose can reduce the sensitivity of target tissues to insulin and therefore can induce type 2 diabetes mellitus in animals (6). The treatment of diabetes relies on the administration of insulin and the taking of oral antidiabetic agents such as metformin, sulphonylureas, glinides, alphaglucosidase inhibitors, etc. ...
Introduction: Combretum molle R.B/G.Don (Combretaceae) is distributed especially in tropical Africa and used in treatment various diseases including diabetes. The aim of the present study was to evaluate the effects of aqueous extract from C. molle boughs (CMAE) on hyperglycemia and dyslipidemia in insulin resistant rats. Methods: Animals were divided into 5 groups and treated for 30 days. Control group received distilled water, sucrose group received 30% sucrose, standard group received 30% sucrose plus metformin (40 mg/kg), and others groups received 30% sucrose plus CMAE (250 and 500 mg/kg). Body weight, food and water intake were evaluated each 10 days for 30 days. Glucose tolerance test was performed on the 30th day of the experiment. Later on, animals were sacrificed and blood was collected for the determination of the concentration of glucose, lipids and insulin. Results: The body weight and food intake of the rats receiving 500 mg/kg of extract decreased significantly on the 30th day of the experiment. CMAE caused a significant reduction of insulin, glucose, cholesterol, triglycerides and low-density lipoprotein cholesterol levels compared to the sucrose lot. However, the extract (250 and 500 mg/kg) showed a significant increase in high-density lipoprotein cholesterol. CMAE induced a significant decrease in postprandial glycaemia. Conclusion: CMAE improved postprandial hyperglycemia and hyperlipidemia in insulin resistant rats.Consequently, CMAE may be able to delay onset of insulin resistance, and reduce the risks and complications of type 2 diabetes.
... Meta-analyses have indicated a strong relationship between sugar consumption and obesity, diabetes, and the metabolic syndrome 3 . However, no definitive studies show an obvious relationship between the intake of total carbohydrates and glycemic control that can lead to type 2 diabetes (T2DM) 4,5 . Many people today usually not only have more sugars but also eat more frequently. ...
Modern lifestyles have altered diet and metabolic homeostasis, with increased sugar intake, glycemic index, and prediabetes. A strong positive correlation between sugar consumption and diabetic incidence is revealed, but the underlying mechanisms remain obscure. Here we show that oral intake of long-term oscillating glucose (LOsG) (4 times/day) for 38 days, which produces physiological glycemic variability in rats, can lead to β-cells gaining metabolic memory in reactive oxygen species (ROS) stress. This stress leads to suppression of forkhead box O1 (FoxO1) signaling and subsequent upregulation of thioredoxin interacting protein, inhibition of insulin and SOD-2 expression, re-expression of Neurog3, and β-cell dedifferentiation and functional failure. LOsG-treated animals develop prediabetes exhibiting hypoinsulinemia and glucose intolerance. Dynamic and timely administration of antioxidant glutathione prevents LOsG/ROS-induced β-cell failure and prediabetes. We propose that ROS stress is the initial step in LOsG-inducing prediabetes. Manipulating glutathione-related pathways may offer novel options for preventing the occurrence and development of diabetes.
... Los hallazgos sugieren que la obesidad y posteriormente la resistencia a la insulina, participan en este proceso y ambas están estrechamente vinculadas [4,39]. El aumento del consumo de fructosa, que comúnmente contienen los alimentos procesados y bebidas sin alcohol, es uno de los factores que contribuyen a la creciente prevalencia de esta patología [24]. ...
El Síndrome Metabólico (SM) es una endocrinopatía asociada
entre otros trastornos sistémicos a la obesidad abdominal, diabetes
mellitus y dislipidemia. El objetivo de este estudio fue determinar
el efecto preventivo de la melatonina sobre el desarrollo del SM
y las alteraciones pancreáticas asociadas. Se seleccionaron 80
ratas Sprague-Dawley machos de 12 semanas de edad, divididos
en 4 grupos de 20: Control, Fructosa, Fructosa más Melatonina
y Melatonina. La inducción del SM se realizó por adición en el
agua de bebida de fructosa al 20% peso/volumen (p/v) durante
28 días (d). Al control se le proporcionó agua pura. La bebida
y el alimento fueron suministrados ad libitum. La melatonina se
administró a una dosis de 3 miligramos (mg)/kilogramos (kg),
vía intraperitoneal (i.p) cada 48 horas (h) durante 28d. El SM se
monitoreó a través de las concentraciones séricas de triglicéridos,
colesterol-HDL, glucosa e insulina, utilizando kits comerciales.
La insulinorresistencia y la funcionalidad de las células beta
pancreáticas fueron determinadas a través del índice HOMA. En
páncreas se realizó el estudio histopatológico y se cuantifcó el
daño lipoperoxidativo. Los datos fueron analizados a través de
un ANOVA y prueba de comparaciones múltiples (P≤0,05).La
administración vía oral de fructosa al 20% durante 28d produjo
hiperglicemia, hipertrigliceridemia, disminución de colesterolHDL,
insulinorresistencia y disminución de la funcionalidad de
la célula beta pancreática, cuadro clínico compatible con el SM.
Igualmente, indujo un aumento signifcativo de la lipoperoxidación
pancreática y una marcada hipertrofa de los islotes pancreáticos.
El tratamiento preventivo con melatonina protegió contra el
desarrollo del SM, evidenciado por la ausencia de los signos
clínicos presentes en los animales que recibieron la sobrecarga
de fructosa, además, la melatonina disminuyó la lipoperoxidación
y preservó la estructura histológica del tejido pancreático. Estos
resultados apuntan al uso de la melatonina como tratamiento
preventivo del SM en los pacientes susceptibles.
... The study of Sievenpiper et al [30] shows that sugar raises blood glucose much faster if it is diluted in water. Over consumption of sucrose have been found to cause weight gain [19] , affects the development of diabetes [31] , and to have adverse effects on glucose tolerance in healthy volunteers [25] . It is now common to find soft drinks and juices replacing formula and milk in children up to 2 years of age [14] . ...
Consumption of sucrose is one of the dietary origins of some health concerns, such as dental caries, obesity and diabetes type 2. In Morocco, the statistics are alarming. Therefore, in order to reduce these major and growing problems of society, substituting sugar with low calorie sweeteners may be effective. Knowing that, the use of these sweetening compounds has increased seriously. Furthermore several experiments have questioned their lack of harmfulness to health, particularly aspartame. The revelation of a potential risk of synthetic sweeteners has led to the emergence of a new market, of intense sweeteners of natural origin, such as stevioside and rebaudioside A. The extracts from the leaves of Stevia rebaudiana Bertoni are natural, sweet-tasting and calorie free that may also be used as a sugar substitute or as an alternative to artificial sweeteners. Much progress has been made concerning their biological and pharmacological effects. This review article summarizes the current scientific researches about the actions and safety of sucrose Aspartame and Stevia rebaudiana extracts on human health.
... METABOLIC SYNDROME (MS) is a cluster of metabolic risk factors that is linked to central obesity, elevated blood pressure, glucose intolerance, and dyslipidemia (30). MS is associated with the risk of developing cardiovascular disease and diabetes and is becoming more common due to changes in lifestyle that include increased consumption of high energetic density foods and sedentary behavior (15,29). Insulin resistance (IR) is considered a key factor in MS pathogenesis, and skeletal muscle damage or wasting is particularly important in IR development once it is responsible for~75-95% of insulinmediated glucose disposal (38). ...
Metabolic Syndrome (MS) is a cluster of metabolic risk factors which is linked to central obesity, elevated blood pressure, insulin resistance (IR) and dyslipidemia, where the rennin-angiotensin system (RAS) may provide a link among them. This study aimed to evaluate volume exercise effects comparing low versus high volume of chronic aerobic exercise on RAS axes in skeletal muscle in a diet-induced obesity (DIO) rat model. For this, male Wistar-Kyoto rats were fed a standard chow diet (SC) or a high-fat diet (HF) for 32 weeks. Animals receiving the HF diet were randomly divided into low exercise volume (LEV, 150 min.week(-1)) and high exercise volume (HEV, 300 min.week(-1)) at the 20(th) week. After 12 weeks of aerobic treadmill training the body mass and composition, blood pressure, glucose and lipid metabolism, RAS axes, insulin signaling and inflammatory pathway were performed. HEV slowed the body mass gain, reduced intra-abdominal fat pad and leptin levels, improved total and peripheral body composition and inflammatory cytokine, reduced AT1R expression and increased Mas receptor protein expression compared with the HF animals. Sedentary groups (SC and HF) presented lower time to exhaustion and maximal velocity compared with the LEV and HEV groups. The both exercise training groups showed reduced resting systolic blood pressure and heart rate, improved glucose tolerance, IR, insulin signaling and lipid profile. We conclude that the HEV, but not LEV, shifted the balance of RAS towards the ACE2/Mas receptor axis in skeletal muscle, presenting protective effects against DIO model.
... These conflicting results might partly be explained by opposite associations of individual mono-and disaccharides with T2DM [2]. The most commonly consumed, and most frequently studied individual mono-and disaccharides are glucose, fructose, and sucrose [3]. In some studies, positive associations of glucose and fructose with prediabetes [4] and T2DM [2,5] have been observed, whereas others revealed inverse [6] or absent associations [7]. ...
The associations of glucose, fructose, and sucrose intake with type 2 diabetes mellitus (T2DM) have been inconsistent. Furthermore, there is a lack of studies focusing on early markers of T2DM that provide insight into the process of T2DM progression: impaired pancreatic β-cell function (BCF) and insulin sensitivity. This study evaluated associations cross-sectionally in a population-based cohort consisting of 2818 individuals (mean ± SD age 59.7 ± 8.18, 49.5% male, n = 120 newly diagnosed T2DM). Glucose, fructose, and sucrose intake were assessed by a food frequency questionnaire. Glucose metabolism status, insulin sensitivity, and BCF were measured by a seven-points oral glucose tolerance test. Linear regression analysis revealed a positive association of glucose intake with insulin sensitivity in the fully adjusted model (standardized beta (95% CI) 0.07 (0.05, 0.14) SD for ≥23 g vs. <10 g of glucose). Fructose and sucrose intake were not associated with insulin sensitivity after full adjustments. In addition, no associations of dietary glucose, fructose, and sucrose with BCF were detected. In conclusion, higher intake of glucose, not fructose and sucrose, was associated with higher insulin sensitivity, independent of dietary fibre. No convincing evidence was found for associations of dietary glucose, fructose, and sucrose with BCF in this middle-aged population.
... Consumption of high quantities of fructose by humans and animals leads to insulin resistance, lipid abnormalities, obesity, hypertension, and renal dysfunction (Araujo et al. 2016;Basciano et al. 2005;Elliott et al. 2002;Farah et al. 2006;Hwang et al. 1987;Laville and Nazare 2009;Sanches et al. 2012;Tappy et al. 2010;). A recent meta-analysis concluded that a fructose intake >50 g/day is associated with altered plasma triglyceride concentrations (Livesey and Taylor 2008). ...
A rapid rise in obesity, as well as physical inactivity, in industrialized countries is associated with fructose-consumption-mediated metabolic syndrome having a strong association with cardiovascular disease. Although insulin resistance is thought to be at the core, visceral obesity, hypertension, and hypertriglyceridemia are also considered important components of this metabolic disorder. In addition, various other abnormalities such as inflammation, oxidative stress, and elevated levels of uric acid are also part of this syndrome. Lifestyle changes through improved physical activity, as well as nutrition, are important approaches to minimize metabolic syndrome and its deleterious effects.
... Sodiumindependent transporter (GLUT4)} (iii) promoting hepatic glucose uptake/utilization/storage and suppression of hepatic glucose production, and (iv) inhibiting lipolysis and promoting lipogenesis in adipose tissue. However, in diabetic conditions, particularly T2DM, insulin-mediated cellular signaling is impaired (insulin resistance) resulting in reduced tissue uptake, reduced suppression of hepatic glucose production, increased plasma glucose concentration in the fasting and/or postprandial state; and while still functioning, increased insulin secretion by the pancreas (eg., hyperinsulinemia) [18]. ...
The incidence of type 2 diabetes mellitus (T2DM) has reached near-epidemic proportions in the Western world with other parts of the world following close behind. Glycemic control is paramount in type 1 diabetes mellitus (T1DM) and T2DM. Berries may beneficially influence glycemic control through the action of their polyphenolic components. While clinical studies on the anti-diabetic effects of berry polyphenols are limited, epidemiological data have indicated favorable effects of berry/anthocyanins intake on development and/or management of T2DM. Furthermore, data derived from in vivo animal studies and in vitro cell culture models are promising. Various molecular targets and modulation of cell signaling pathways in pancreatic β-cells, hepatocytes, adipocytes, and skeletal muscle cells are among the proposed mechanisms for berry polyphenols and their metabolites' action. Berry polyphenols may exert anti-diabetic effects by (i) enhancing insulin production and reducing apoptosis and promoting proliferation of pancreatic β-cells, (ii) regulating glucose metabolism by interfering with absorption or by increasing peripheral tissue glucose uptake through insulin receptor-dependent or independent mechanisms via modification of oxidative stress, inflammation or perceived energy status of cell. This mini review discusses recent findings from our laboratory and other studies on the anti-diabetic effects of berry polyphenolic compounds with special emphasis on the cellular and molecular mechanisms involved in the beneficial effects of berry polyphenol compounds.
... Numerous studies show that the form in which sugars are ingested and the frequency of their consumption are directly related to the prevalence of caries [17]. Sugars also contribute to the increase in an elevated number of health problems such as obesity and dysmetabolic diseases [18,19]. ...
Abstract: Stevia rebaudiana Bertoni is a small perennial shrub of the Asteraceae (Compositae) family
that is native to South America, particularly Brazil and Paraguay, where it is known as “stevia” or
“honey leaf” for its powerful sweetness. Several studies have suggested that in addition to their
sweetness, steviosides and their related compounds, including rebaudioside A and isosteviol, may
offer additional therapeutic benefits. These benefits include anti-hyperglycaemic, anti-hypertensive,
anti-inflammatory, anti-tumor, anti-diarrheal, diuretic, and immunomodulatory actions. Additionally,
critical analysis of the literature supports the anti-bacterial role of steviosides on oral bacteria flora.
The aim of this review is to show the emerging results regarding the anti-cariogenic properties of
S. rebaudiana Bertoni. Data shown in the present paper provide evidence that stevioside extracts from
S. rebaudiana are not cariogenic. Future research should be focused on in vivo studies to evaluate the
effects on dental caries of regular consumption of S. rebaudiana extract-based products.
Keywords: Stevia rebaudiana Bertoni; dental caries; sweetener
Integrating light-emitting diode (LED) lighting systems in greenhouse and plant hydroponic culture represents a significant stride towards sustainable agriculture. This study explores the pivotal role of LED technology, particularly for purple, blue, and red light in nurturing to enhance plant growth and development. Plant photoreceptors absorb different wavelengths of light and activate a signaling cascade from upstream to downstream that will activate several complex physiological processes and morphogenesis. Red light (R, 620–700 nm) is recognized by phytochrome which controls photomorphogenesis via promoting vegetative and generative growth and development including germination, flowering and fruiting. On the other hand, blue light (B, 445–500 nm) is recognized by cryptochromes which stimulate photosynthesis, chlorophyll - carotenoids biosynthesis, and stomatal opening. In terms of nutritional quality, applying B light to plants can increase the accumulation of anthocyanins, carotenoids, and ascorbic acid contents. R lights determine better growth compared to B lights. Furthermore, adding B light to R light as a combination at low intensity can prevent excessive etiolation and reactivate chlorophyll synthesis. In addition, it has been reported that the combination of R and B light increases the development of photosynthetic apparatus, accumulation of biomass, forming more compact plant structure and inhibits flowering. The efficiency of absorption and assimilation of macro and micronutrients in hydroponic systems is also stimulated by the combination of R and B light. Combining R and B in balanced percentages can form purple light fixtures. Purple light is commonly used in the early stages of growth to induce seed germination, cell division and shoot regeneration. A combination of R and B light for LED lighting in the greenhouse and hydroponic culture systems may provide improved control of the crop growing environment and reduce pollutant emissions, producing a homogeneous and high-quality crop, time efficient and low-cost production with predictable results. Through this farming strategy, LED-equipped facilities maximize spatial efficiency and become a solution for obtaining efficient yields and high nutritional value, thus providing a strong case for integrating them into future modern agricultural practices.
Circular RNAs (circRNAs) are a large family of closed-loop RNA molecules emerging as novel regulators of gene expression. Although several circRNAs are known to regulate various biological processes, the functions of most circRNAs expressed in pancreatic beta cells remain to be discovered. Since short-term glucose treatment induces pancreatic beta-cell growth and promotes insulin production, we wanted to explore the role of glucose-regulated circRNAs in pancreatic beta cell physiology. Our RNA-seq analysis identified more than 300 differentially expressed circRNAs in high-glucose compared to low-glucose treated beta TC6 cells. A subset of differentially expressed and abundant circRNAs was validated by various biochemical methods, including circular RNA Rabep1 (circRabep1). Moreover, the downregulation of circRabep1 in high glucose-treated beta TC6 cells suggested a possible function in beta-cell physiology. Furthermore, analysis of the circRabep1-miRNA-mRNA regulatory network discovered the association of circRabep1 with miR-335-3p, a suppressor of Pten expression. Importantly, inhibition of miRNA function by miR-335-3p inhibitor results in upregulation of PTEN levels, suppressing beta-cell growth and proliferation. Furthermore, silencing circRabep1 decreased PTEN expression by sponging miR-335-3p, promoting cell proliferation. We propose that the downregulation of circRabep1 in high-glucose treated beta-cell leads to an increase in beta-cell proliferation by suppressing PTEN expression through derepression of miR-335-3p.
Aim
To explore the link between the RBP4 rs3758539 genotype and metabolic syndrome risk factors and whether the impact of this genetic variation displays any potential race discrepancy.
Materials and Methods
This meta‐analysis followed the PRISMA guidelines and was registered with PROSPERO (registration no. CRD42023407999). PubMed, Web of Science, Embase, Cochrane Library, Google Scholar, Airiti Library and CINAHL databases were used for the study search until October 2023. We evaluated the methodological quality using the Joanna Briggs Institute checklist and determined the correlation using a random‐effects meta‐analysis.
Results
The results indicated that individuals with the rs3758539 GA/AA genotype had a higher risk profile, including lower high‐density lipoprotein levels [correlation: −0.045, 95% confidence interval (CI): −0.080 to −0.009, p = .015, I ² = 46.9%] and higher body mass index (correlation: 0.117, 95% CI: 0.036‐0.197, p = .005, I ² = 82.0%), body fat (correlation: 0.098, 95% CI: 0.004‐0.191, p = .041, I ² = 64.0%), and low‐density lipoprotein levels (correlation: 0.074, 95% CI: 0.010‐0.139, p = .024, I ² = 0%), of developing metabolic syndrome than those with the GG genotype. The subgroup analysis maintained a significantly positive correlation between the rs3758539 GA/AA genotype and body mass index (correlation: 0.163, 95% CI: 0.031‐0.289, p = .016, I ² = 88.9%) but a negative correlation with high‐density lipoprotein levels (correlation: −0.047, 95% CI: −0.087 to −0.006, p = .025, I ² = 65.7%) in the Asian group only.
Conclusion
The current meta‐analysis supports a significant link between the RBP4 rs3758539 GA/AA genotype and the metabolic syndrome.
Artificially sweetened beverages containing noncaloric monosaccharides were suggested as healthier alternatives to sugar-sweetened beverages. Nevertheless, the potential detrimental effects of these noncaloric monosaccharides on blood vessel function remain inadequately understood. Presently, we have established a zebrafish model that exhibits significant excessive angiogenesis induced by high glucose, resembling the hyperangiogenic characteristics observed in proliferative diabetic retinopathy (PDR). Utilizing this model, we observed that glucose and noncaloric monosaccharides could induce excessive formation of blood vessels, especially intersegmental vessels (ISVs). The excessively branched vessels were observed to be formed by ectopic activation of quiescent endothelial cells (ECs) into tip cells. Single-cell transcriptomic sequencing analysis of the endothelial cells in the embryos exposed to high glucose revealed an augmented ratio of capillary ECs, proliferating ECs, and a series of upregulated proangiogenic genes. Further analysis and experiments validated that foxo1a mediated the excessive angiogenesis induced by monosaccharides by down-regulating the expression of marcksl1a . This study has provided new evidence showing the negative effects of noncaloric monosaccharides on the vascular system and the underlying mechanisms.
Insulin resistance is an important feature of metabolic syndrome and a precursor of type 2 diabetes mellitus (T2DM). Overnutrition-induced obesity is a major risk factor for the development of insulin resistance and T2DM. The intake of macronutrients plays a key role in maintaining energy balance. The components of macronutrients distinctly regulate insulin sensitivity and glucose homeostasis. Precisely adjusting the beneficial food compound intake is important for the prevention of insulin resistance and T2DM. Here, we reviewed the effects of different components of macronutrients on insulin sensitivity and their underlying mechanisms, including fructose, dietary fiber, saturated and unsaturated fatty acids, and amino acids. Understanding the diet-gene interaction will help us to better uncover the molecular mechanisms of T2DM and promote the application of precision nutrition in practice by integrating multi-omics analysis.
Background & aims:
Type 2 diabetes mellitus (T2DM) is a common endocrine disease. Altered gut microbiota (Dysbiosis) is closely associated with development of T2DM. Growing body of evidence hypothesized that probiotics intake may be useful for patients with T2DM. We investigated the effect of probiotic yogurt consumption on glycemic control and lipid profile in patients with T2DM.
Methods:
In this 12-week randomized controlled clinical trial, seventy-two patients with T2DM were randomly assigned to the intervention group (IG) that received 200 g/d probiotic yogurt containing 4.65 × 106 CFU/g Lactobacillus acidophilus and Bifidobacterium lactis) or placebo group (PG) that received 200 g/d conventional yogurt.
Results:
We found no difference between two groups in fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-c) and low density lipoprotein-cholesterol (LDL-c) after intervention. After adjusting for baseline values of covariate, a significant reduction in HbA1c (mean change: -0.76 ± 1.3 vs. -0.15 ± 1.3; P = 0.01), TC (mean change: -10.61 ± 27.8 vs. -2.97 ± 35.0; P = 0.02) and LDL-c (mean change: -8.62 ± 21.7 vs. 0.02 ± 25.8; P = 0.004) was observed in the IG compared to the PG. In addition, a non-significant trend to reduction was observed in term of FPG (mean change: -19.61 ± 29.1 vs. -4.19 ± 24.2; P = 0.13). TG and HDL-c remained unchanged.
Conclusions:
Probiotic yogurt consumption may be useful for patients with T2DM. More well-designed clinical trials with longer intervention duration are required. Registered on 30 July 2022 at Iranian Registry of Clinical Trials (IRCT20220226054125N1) with URL: https://www.irct.ir/trial/62304.
Aims
Reduced cardiac autophagy, ischemic injury, sympathetic overactivity, and apoptosis all contribute to metabolic syndrome (MetS)-associated cardiovascular risks. NR4A2, an orphan nuclear receptor NR4A family member, induces autophagy while suppressing apoptosis in myocardial infarction. Moxonidine, a sympathoinhibitor imidazoline1 receptor (I1R) agonist, has beneficial metabolic and hemodynamic effects; however, whether autophagy and/o NR4A2 signaling are involved moxonidine's cardiovascular effects via I1R activation, is unknown, and is the aim of this study.
Materials and methods
To induce MetS, rats were fed 3 % salt in their diet and 10 % fructose in their drinking water for 12 weeks. MetS-rats were given either moxonidine (6 mg/kg/day, gavage), efaroxan (I1R antagonist, 0.6 mg/kg/day, i.p), both treatments, or vehicles for the last two weeks. Blood pressure, lipid profile, and glycemic control were evaluated. Histopathological examination, circulating cardiac troponin I (c-TnI), proinflammatory interleukin-6 (IL-6), apoptosis (active caspase-3 and Fas-immunostaining), interstitial fibrosis [transforming growth factor-β1 (TGF-β1) and Mallory's trichrome staining], and extracellular matrix remodeling [matrix metalloproteinase-9 (MMP-9)], were used to assess cardiac pathology. Cardiac NR4A2 and its downstream factor, P53, as well as autophagic flux markers, SQSTM1/p62, LC3, and Beclin-1 were also determined.
Key findings
Moxonidine significantly ameliorated MetS-induced metabolic and hemodynamic derangements and the associated cardiac pathology. Moxonidine restored NR4A2 and P53 myocardial levels and enhanced autophagic flux via modulating LC3, Beclin-1, and SQSTM1/p62. Efaroxan reversed the majority of the moxonidine-induced improvements.
Significance
The current study suggests that autophagy modulation via I1R activation is involved in moxonidine-mediated cardiac beneficial effects in MetS.
Objective: This study aimed to evaluate the differential role of a high-fat diet (HF) or high-fructose diet (HFRU) on white adipose tissue and brown adipose tissue remodeling in C57BL/6 mice.Methods: The animals were randomly assigned to receive HF (50% of energy as lipids), HFRU (50% of energy as fructose), or a control diet (C, 10% of energy as lipids) for 12 weeks. Results: The HF group became overweight from the 7th week onwards, but both HF and HFRU groups showed hyperinsulinemia, oral glucose intolerance, and adverse adipose tissue remodeling. HF and HFRU groups showed interscapular brown adipose tissue whitening, tough the reduced QA [nuclei] suggested maximized brown adipocyte dysfunction due to the HFRU diet. In contrast, HF and HFRU diets exerted similar effects upon subcutaneous white adipocytes, with a similar average cross-sectional area. Immunohistochemistry confirmed the whitening enhancement with reduced UCP1 immunodensity in the HFRU group. Conclusion: In conclusion, HF and HFRU diets had indistinguishable effects upon white adipocyte morphology, but the HFRU diet provoked a more pronounced whitening than the HF diet after a 12-week protocol. These results point to the silent and harmful impact that excessive fructose has upon the metabolism of lean mice.
Background and Aims
Non-alcoholic fatty liver disease (NAFLD) as the most common chronic liver disease is closely linked to type 2 diabetes mellitus (T2DM). Omega-3 supplementation has been proposed as a strategy to manage T2DM and NAFLD. The present study aimed to investigate the effect of omega-3 supplementation on fatty liver index, lipid accumulation product and visceral adiposity index in diabetic patients with NAFLD.
Methods
In this 12-week double-blind, randomized controlled clinical trial, sixty diabetic patients with NAFLD were randomly assigned into the omega-3 and placebo groups for 12 weeks. The omega-3 group received 2000 mg/d omega-3 as capsule.
Results
Fifty-six participants completed the study. No significant difference was found between the two groups in the terms of fatty liver index, lipid accumulation product and visceral adiposity index at the baseline. Omega-3 supplementation compared with the placebo led to a significant improvement in fatty liver index (-3.6 ± 12.1 vs. 0.9 ± 8.9; P = 0.04), lipid accumulation product (-14.2 ± 27.9 vs. 8.0 ± 26.3; P = 0.002) and visceral adiposity index (-0.5 ± 0.9 vs. 0.0 ± 0.8; P = 0.01).
Conclusion
Omega-3 supplementation for 12 weeks improves fatty liver index, lipid accumulation product and visceral adiposity index. The study protocol was registered under Iranian Registry of Clinical Trials identifier number IRCT2016102530489N1.
The purpose of this study was to perform a literature review about diabetes mellitus 2 to characterize the main root cause and the best strategies for solution and prevention in the educational processes. The analysis was performed using the Eight Disciplines Problem Solving Method. To this end, a script was prepared based on the definition of the concepts of interest. The search criteria for data were also defined. The information was subsequently selected using these criteria. This study identified the containment measures and the social determinants that minimize them and the main solutions for practical application at the primary care level. The relevance of changes in educational processes based on the cause main root were examined for non-communicable diseases, addition of fructose to soft drinks, and foods made by the food industry. The results showed that diabetes and obesity are not the result of simple calorie imbalance. Good health depends on traditional ethnic dishes. These concepts should be incorporated into the training processes of health professionals.
Scope:
This review represents a focus on the structure and properties of the common nutritional disaccharides (lactose, maltose and sucrose) in health and disease. The aim is to provide a comprehensive reference source related to the role of disaccharides in human nutrition.
Methods and results:
Key reference sources were searched including Web of Science, PubMed, Science Direct, Wiley Online etc. and key reference works were selected to support the factual basis of the text where interpretations and relevance of the works were discussed in the review. There are key nutritional health benefits of receiving dietary energy in the form of sugars but equally life-threatening issues exist associated with constant/excess consumption. These issues are discussed together with genetic disorders which impact upon health associated with consumption of the disaccharides (e.g., specific disaccharide intolerance due to deficiency of relevant digestive enzymes).
Conclusions:
As the three common dietary disaccharides (lactose, maltose and sucrose) are consumed on a very regular basis in the human diet, it is critical to understand insofar as possible their role in health and disease. This review provides an insight into the structure and properties of these molecules in health and disease. This article is protected by copyright. All rights reserved.
Fruits come in a wide variety of colors, shapes, and flavors. This chapter will cover selected fruits that are known to be healthy and highly nutritious. These fruits were chosen due to their common usage and availability. Since it is not possible to cover all health benefits or essential nutrients and important phytochemicals of the fruit composition, this chapter will focus on the key valuable constituents and their potential health effects.
Yacon (Smallanthus sonchifolius Poepp. & Endl.) as an underutilized crop, native to the Andean region, has attracted growing attention. The tuberous roots of yacon have been advertised as an alternative low caloric plant source for replacing sucrose. In fact, yacon has gained recognition based on the fact that its sweet tasting tuberous roots and its leaves have a favourable phytochemical content to be included in a range of functional food products. The leaves on the one hand are a significant source of health promoting phenolic compounds and their extract exerts certain biological activities such as antioxidant activity and hyperglycemic effects. The tubers on the other hand consist of carbohydrates including simple sugars, namely, fructose, glucose, sucrose and fructooligosaccharides (FOS). The FOS - representing the dominant polysaccharide in the tubers - are sweet tasting, prebiotic, and non-digestible oligosaccharides. Therefore, their consumption imposes several health benefits such as lowering the energy intake while enhancing the beneficial microflora of the colon. It is noted that 60-70 % of the dry matter content of yacon tubers is composed of FOS. Besides, yacon tubers are a remarkable source of biological components such as phenolic compounds. Thus, yacon is considered as multifunctional plant food. The main objectives of this thesis were to 1) differentiate between the quality of young and old yacon leaves of two cultivars (red and white) in terms of their total phenolic content (TPC), total flavonoid content (TFC), antioxidant activity when using ohmic-assisted decoction (OH-DE) and decoction (DE) as well as energy consumption of extraction process, 2) differentiate between various parts of yacon tubers (flesh, peel and whole tuber) of seven cultivars in terms of their simple sugar (fructose, glucose and sucrose) content, TPC, TFC and antioxidant activity, 3) examine the TPC and antioxidant activity of yacon tubers of two cultivars (red and white) one week and three weeks after the harvest and under the influence of different pre-treatments before drying, and 4) determine the effect of drying on quality of yacon chips produced from two cultivars (red and white) at two time intervals after harvest. Overall, this thesis provided a broad dataset und information with regard to phytochemical contents of yacon leaves and tubers of different cultivars grown under the environmental conditions of southwestern Germany. However, further studies with regard to the determination of individual functional constitutes of leaves and tubers of yacon, their mechanism of action and effectiveness in promoting the health benefits, and their safety is essential. Moreover, with regard to novel product development from yacon leaves and tubers, further studies are strongly suggested to ensure the sustainability of final food products by optimizing energy consumption and environmental impacts of the whole food supply chain for such products as well as their quality.
High-fat and high-sucrose intakes were shown to contribute to syndromes such as hyperlipidemia, glucose intolerance, hypertension, and atherosclerosis. The pathogenesis of such diseases caused by high-fat and/or high-sucrose diet is unclear. The aim of the present study was to investigate plasma microRNA expression profiling in high-fat and high-sucrose fed rats. In total, 28 adult Wistar albino postnatal (8–12 weeks) male rats were involved in this experiment. The experimental animals were randomly divided four groups and fed with either standard rat chow, high-fat diet, high-sucrose diet and high-fat & high-sucrose diet for a period of 4 weeks. miRNAs were extracted from plasma and detected to miRNA expression profiling (Eighty four miRNAs) by quantitative real-time PCR (qRT-PCR) with the Fluidigm integrated microfluidic circuit technolog.
Among miRNAs, expression profiles of twenty miRNAs were found to be significantly different (P < 0,05) between groups. Of these twenty miRNAs, 1 were upregulated and 19 were downregulated with high-fat and high-sucrose feeding. The following miRNAs were downregulated: miR-130a-3p, miR-320-3p, miR-17-5p, miR-16-5p, miR-144-3p, miR-93-5p, miR-192-5p, miR-532-5p, miR-106b-5p, miR-26b-5p, miR-208b-3p, miR-23a-3p, miR-25-3p, miR-15b-5p, miR-195-5p, miR-103-3p, miR-122-5p, miR-29b-3p and miR-30a-3p and the following miRNAs were upregulated: miR-375-5p.
These results indicate that aberrant expression of miRNA profiles may be associated with the development of hyperlipidemia, insulin resistance and cancer in the high-fat & high-sucrose-fed rat.
We optimized the assays used to measure inhibition of rat and human α-glucosidases (sucrase and maltase activities), intestinal enzymes which catalyze the final steps of carbohydrate digestion. Cell-free extracts from fully differentiated intestinal Caco-2/TC7 monolayers were shown to be a suitable source of sucrase-isomaltase, with the same sequence as human small intestine, and were compared to a rat intestinal extract. The kinetic conditions of the assay were optimized, including comparison of enzymatic and chromatographic methods to detect the monosaccharide products. Human sucrase activity was more susceptible than the rat enzyme to inhibition by acarbose (IC50 (concentration required for 50% inhibition) = 2.5 ± 0.5 and 12.3 ± 0.6 μM, respectively), by a polyphenol-rich green tea extract, and by pure (-)-epigallocatechin gallate (EGCG) (IC50 = 657 ± 150 and 950 ± 86 μM respectively). In contrast, the reverse was observed when assessing maltase activity (e.g.
, egcg:
IC50 = 677 ± 241 and 14.0 ± 2.0 μM for human and rat maltase, respectively). 5-Caffeoylquinic acid did not significantly inhibit maltase and was only a very weak inhibitor of sucrase. The data show that for sucrase and maltase activities, inhibition patterns of rat and human enzymes are generally qualitatively similar but can be quantitatively different.
This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects of fructose substitution of glucose or sucrose in food for normoglycaemic persons or people with or at risk of diabetes.
The best illustration of the gene-diet interaction in nature is the process that generates queen bee and worker bees from larvae, by the selective feeding of royal jelly (Shi et al. 2011). Optimal timing of the nutrients affects the body composition and longevity of the bee. The polyunsaturated fatty acids in the pollen transform the larvae to worker bees, whereas the queen bee is always fed mouth-to-mouth with the royal jelly, which is devoid of polyunsaturates (Hulbert 2010). The literature on diet and cardiovascular health has exponentially increased and does address the finer details (Bhupathiraju and Tucker 2011; Brunner et al. 2008; Daniels et al. 2011; Krachler et al. 2009; Lichtenstein et al. 2006; Marques-Vidal et al. 2004; Mente et al. 2009; Mozaffarian and Capewell 2011; Simopoulos 2001; Sivasankaran 2010; Stamler 2008; Tada et al. 2011; Weintraub et al. 2011). Diet is what we eat; nutrition is what the body gets, but the outcome depends on how our body responds. The importance of traditional diets is well stressed in dietary guidelines as exemplified by the healthy aging seen with Mediterranean diets and in Okinawa islanders of Japan (Bonaccio et al. 2012; Lichtenstein et al. 2006; Sho 2001; Speakman and Mitchell 2011; Willcox et al. 2006; Willett 2006). Given the personal preferences in dietary choices that please the mind and taste buds, dietary guidelines are only good science that needs to be modified by common sense. But marketing strategies of the food industry easily spoil these choices (Scott 2005). Ideal diets are ones that promote health and longevity so that we live to our biological potential (Alpert 2001; Chahoud et al. 2004). It is never too late to adopt this lifestyle modification, since the benefit accrued is rapid and substantial (Capewell and O’Flaherty 2011). Tackling the issues of unhealthy diets is likely to halve the current cardiovascular disease (CVD) epidemic, and give additional benefits in terms of related diseases like obesity, diabetes, and cancer (Mozaffarian and Capewell 2011). This chapter takes you through an interesting journey starting with food processing, evolutionary aspects of diet, and preventive strategies, through the lifecycle effects of nutrition, to provide the reader the scientific background behind the heart-healthy diet plate.
This is the protocol for a review and there is no abstract. The objectives are as follows: To assess the effects of fructose substitution of glucose or sucrose in food for normoglycaemic persons or people with impaired glucose tolerance or diabetes.
The prevalence of diabetes, obesity, and hypertension in the United States is concerning. The etiologies of these chronic diseases are multifactorial in nature, involving varying genetic, social, and environmental factors. The relationship between food and food ingredients and risk for chronic disease has been particularly questioned. Specifically, scientific investigators have extensively examined the relationship between sugars and health. Consensus to date includes the following: total sugar intake does not cause type 2 diabetes; evidence linking sugar consumption to obesity is inconsistent; and intake of carbohydrates, including sugars, is not considered an independent risk factor for cardiovascular disease. Although more research is needed in some areas, in general, the available data show no direct link between moderate consumption of sugars and serious diseases or obesity.
Insulin resistance is associated with diabetes mellitus, ischemic heart disease, and hypertension both independently and as part of syndrome X. Environmental influences on SI are incompletely understood. Exercise has a strong beneficial effect and obesity a strong adverse effect. The balance of evidence suggests that a high-fat diet is likely to reduce insulin sensitivity but the effects of dietary carbohydrates are more controversial. Extensive studies in animals showed a detrimental effect of diets very high in fructose or sucrose, particularly in association with induction of hypertriglyceridemia. The more limited studies in humans had conflicting results, partly because of heterogeneity of design. Certain groups of subjects may be more sensitive to adverse effects of high intakes of dietary sucrose or fructose. More carefully controlled studies in humans are needed to provide evidence on which to base public health policies with respect to dietary carbohydrates and SI.
Objective:
To examine prospectively the relationship between glycemic diets, low fiber intake, and risk of non-insulin-dependent diabetes mellitus.
Design:
Cohort study.
Setting:
In 1986, a total of 65173 US women 40 to 65 years of age and free from diagnosed cardiovascular disease, cancer, and diabetes completed a detailed dietary questionnaire from which we calculated usual intake of total and specific sources of dietary fiber, dietary glycemic index, and glycemic load.
Main outcome measure:
Non-insulin-dependent diabetes mellitus.
Results:
During 6 years of follow-up, 915 incident cases of diabetes were documented. The dietary glycemic index was positively associated with risk of diabetes after adjustment for age, body mass index, smoking, physical activity, family history of diabetes, alcohol and cereal fiber intake, and total energy intake. Comparing the highest with the lowest quintile, the relative risk (RR) of diabetes was 1.37 (95% confidence interval [CI], 1.09-1.71, P trend=.005). The glycemic load (an indicator of a global dietary insulin demand) was also positively associated with diabetes (RR= 1.47; 95% CI, 1.16-1.86, P trend=.003). Cereal fiber intake was inversely associated with risk of diabetes when comparing the extreme quintiles (RR=0.72, 95% CI, 0.58-0.90, P trend=.001). The combination of a high glycemic load and a low cereal fiber intake further increased the risk of diabetes (RR=2.50, 95% CI, 1.14-5.51) when compared with a low glycemic load and high cereal fiber intake.
Conclusions:
Our results support the hypothesis that diets with a high glycemic load and a low cereal fiber content increase risk of diabetes in women. Further, they suggest that grains should be consumed in a minimally refined form to reduce the incidence of diabetes.
OBJECTIVE: To investigate the long-term effects of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates.DESIGN: Randomized controlled multicentre trial (CARMEN), in which subjects were allocated for 6 months either to a seasonal control group (no intervention) or to one of three experimental groups: a control diet group (dietary intervention typical of the average national intake); a low-fat high simple carbohydrate group; or a low-fat high complex carbohydrate group.SUBJECTS: Three hundred and ninety eight moderately obese adults.MEASUREMENTS: The change in body weight was the primary outcome; changes in body composition and blood lipids were secondary outcomes.RESULTS: Body weight loss in the low-fat high simple carbohydrate and low-fat high complex carbohydrate groups was 0.9 kg (P
BACKGROUND: High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated. OBJECTIVE: We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7). DESIGN: IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy. RESULTS: Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the high-fructose diet (r = -0.78, P < 0.05). CONCLUSION: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.
In South Asians (Indians, Pakistanis, and Bangladeshis) settled overseas, high rates of coronary disease and non-insulin-dependent diabetes occur in association with central obesity and insulin resistance. To examine whether these disturbances were related to diet, we measured 7-d weighed intakes in 173 South Asian and European men aged 40-69 y in London. In South Asians compared with Europeans, respectively, mean energy intake was lower (9.5 vs 10.8 MJ/day, P < 0.001), total fat intake was lower (36.5% vs 39.2% of energy intake, P = 0.007), starch intake was higher (28.0% vs 21.5% of energy, P < 0.001), polyunsaturated fatty acid intake was higher (8.2% vs 7.0% of energy, P = 0.02), and dietary fiber intake was higher (3.2 vs 2.0 g/MJ, P < 0.001). Elevated serum insulin concentrations at 2 h postglucose were associated positively with carbohydrate intake (P = 0.001) and inversely with alcohol intake (P = 0.006), but not with saturated fatty acid intake. The high coronary risk in South Asian people is not explained by any unfavorable characteristic of South Asian diets.
Fructose absorption was studied by the breath hydrogen test in 114 healthy children aged 0.1-6 years, given either 2 g/kg or 1 g/kg of fructose. All 57 children given 2 g/kg had peak breath hydrogen excretions > or = 20 ppm. At 1 g/kg only 25/57 (44%) showed incomplete absorption and the percentage incompletely absorbing fructose and the peak breath hydrogen value were significantly higher in children aged 1-3 years. Interestingly, this age distribution correlates with that of toddler diarrhoea.
The cellular basis of insulin resistance is still unknown; however, relationships have been demonstrated between insulin action in muscle and the fatty acid profile of the major membrane structural lipid (phospholipid). The present study aimed to further investigate the hypothesis that insulin action and adiposity are associated with changes in the structural lipid composition of the cell. In 52 adult male Pima Indians, insulin action (euglycemic clamp), percentage body fat (pFAT; underwater weighing), and muscle phospholipid fatty acid composition (percutaneous biopsy of vastus lateralis) were determined. Insulin action (high-dose clamp; MZ) correlated with composite measures of membrane unsaturation (% C20-22 polyunsaturated fatty acids [r= 0.463, P < 0.001], unsaturation index [r= -0.369, P < 0.01]), a number of individual fatty acids and with delta5 desaturase activity (r= 0.451, P < 0.001). pFAT (range 14-53%) correlated with a number of individual fatty acids and delta5 desaturase activity (r= -0.610, P < 0.0001). Indices of elongase activity (r= -0.467, P < 0.001), and delta9 desaturase activity (r= 0.332, P < 0.05) were also related to pFAT but not insulin action. The results demonstrate that delta5 desaturase activity is independently related to both insulin resistance and obesity. While determining the mechanisms underlying this relationship is important for future investigations, strategies aimed at restoring "normal" enzyme activities, and membrane unsaturation, may have therapeutic importance in the "syndromes of insulin resistance."
Intake of carbohydrates that provide a large glycemic response has been hypothesized to increase the risk of NIDDM, whereas dietary fiber is suspected to reduce incidence. These hypotheses have not been evaluated prospectively.
We examined the relationship between diet and risk of NIDDM in a cohort of 42,759 men without NIDDM or cardiovascular disease, who were 40-75 years of age in 1986. Diet was assessed at baseline by a validated semiquantitative food frequency questionnaire. During 6-years of follow-up, 523 incident cases of NIDDM were documented.
The dietary glycemic index (an indicator of carbohydrate's ability to raise blood glucose levels) was positively associated with risk of NIDDM after adjustment for age, BMI, smoking, physical activity, family history of diabetes, alcohol consumption, cereal fiber, and total energy intake. Comparing the highest and lowest quintiles, the relative risk (RR) of NIDDM was 1.37 (95% CI, 1.02-1.83, P trend = 0.03). Cereal fiber was inversely associated with risk of NIDDM (RR = 0.70; 95% CI, 0.51-0.96, P trend = 0.007; for > 8.1 g/day vs. < 3.2 g/day). The combination of a high glycemic load and a low cereal fiber intake further increased the risk of NIDDM (RR = 2.17, 95% CI, 1.04-4.54) when compared with a low glycemic load and high cereal fiber intake.
These findings support the hypothesis that diets with a high glycemic load and a low cereal fiber content increase risk of NIDDM in men. Further, they suggest that grains should be consumed in a minimally refined form to reduce the incidence of NIDDM.
Insulin resistance is associated with diabetes mellitus, ischemic heart disease, and hypertension both independently and as part of syndrome X. Environmental influences on SI are incompletely understood. Exercise has a strong beneficial effect and obesity a strong adverse effect. The balance of evidence suggests that a high-fat diet is likely to reduce insulin sensitivity but the effects of dietary carbohydrates are more controversial. Extensive studies in animals showed a detrimental effect of diets very high in fructose or sucrose, particularly in association with induction of hypertriglyceridemia. The more limited studies in humans had conflicting results, partly because of heterogeneity of design. Certain groups of subjects may be more sensitive to adverse effects of high intakes of dietary sucrose or fructose. More carefully controlled studies in humans are needed to provide evidence on which to base public health policies with respect to dietary carbohydrates and SI.
To investigate the long-term effects of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates.
Randomized controlled multicentre trial (CARMEN), in which subjects were allocated for 6 months either to a seasonal control group (no intervention) or to one of three experimental groups: a control diet group (dietary intervention typical of the average national intake); a low-fat high simple carbohydrate group; or a low-fat high complex carbohydrate group.
Three hundred and ninety eight moderately obese adults.
The change in body weight was the primary outcome; changes in body composition and blood lipids were secondary outcomes.
Body weight loss in the low-fat high simple carbohydrate and low-fat high complex carbohydrate groups was 0.9 kg (P < 0.05) and 1.8 kg (P < 0.001), while the control diet and seasonal control groups gained weight (0.8 and 0.1 kg, NS). Fat mass changed by -1.3kg (P< 0.01), -1.8kg (P< 0.001) and +0.6kg (NS) in the low-fat high simple carbohydrate, low-fat high complex carbohydrate and control diet groups, respectively. Changes in blood lipids did not differ significantly between the dietary treatment groups.
Our findings suggest that reduction of fat intake results in a modest but significant reduction in body weight and body fatness. The concomitant increase in either simple or complex carbohydrates did not indicate significant differences in weight change. No adverse effects on blood lipids were observed. These findings underline the importance of this dietary change and its potential impact on the public health implications of obesity.
Little is known about the variation of the glycemic index (GI) in the diet of European outpatients with type 1 diabetes and how the GI of a commonly consumed diet is associated with metabolic control.
The present study examined the calculated dietary GI of European outpatients with type 1 diabetes for possible relations to glycated hemoglobin (Hb A(1c)) and serum lipid concentrations.
The relation of the GI (calculated from a 3-d dietary record) to Hb A(1c), serum cholesterol (total, LDL, and HDL), and fasting triacylglycerol was analyzed in 2810 people with type 1 diabetes from the EURODIAB Complications Study.
The GI was independently related to Hb A(1c) (P = 0.0001). Compared with the highest GI quartile (median GI: 89), adjusted Hb A(1c) in the lowest GI quartile (median GI: 75) was 11% lower in patients from southern European centers and 6% lower in patients from northern, western, and eastern European centers. Of the serum lipids, only the HDL cholesterol in patients from these European centers was independently related to the GI (P = 0.002). In southern European centers, the consumption of pasta, temperate-climate fruit, white bread, and potatoes largely determined the patients' dietary GI, whereas in the northern, western, and eastern European centers, consumption of bread, potatoes, and temperate-climate fruit was most relevant.
This study in European patients with type 1 diabetes showed that a lower dietary GI is related to lower Hb A(1c) concentrations, independently of fiber intake. The consumption of bread and pasta had the biggest effect on the overall dietary GI of European outpatients.
Previous studies have examined individual dietary and lifestyle factors in relation to type 2 diabetes, but the combined effects of these factors are largely unknown.
We followed 84,941 female nurses from 1980 to 1996; these women were free of diagnosed cardiovascular disease, diabetes, and cancer at base line. Information about their diet and lifestyle was updated periodically. A low-risk group was defined according to a combination of five variables: a bodymass index (the weight in kilograms divided by the square of the height in meters) of less than 25; a diet high in cereal fiber and polyunsaturated fat and low in trans fat and glycemic load (which reflects the effect of diet on the blood glucose level); engagement in moderate-to-vigorous physical activity for at least half an hour per day; no current smoking; and the consumption of an average of at least half a drink of an alcoholic beverage per day.
During 16 years of follow-up, we documented 3300 new cases of type 2 diabetes. Overweight or obesity was the single most important predictor of diabetes. Lack of exercise, a poor diet, current smoking, and abstinence from alcohol use were all associated with a significantly increased risk of diabetes, even after adjustment for the body-mass index. As compared with the rest of the cohort, women in the low-risk group (3.4 percent of the women) had a relative risk of diabetes of 0.09 (95 percent confidence interval, 0.05 to 0.17). A total of 91 percent of the cases of diabetes in this cohort (95 percent confidence interval, 83 to 95) could be attributed to habits and forms of behavior that did not conform to the low-risk pattern.
Our findings support the hypothesis that the vast majority of cases of type 2 diabetes could be prevented by the adoption of a healthier lifestyle.
To investigate prospectively whether intake of total or type of sugar is associated with the risk of developing type 2 diabetes. The contribution of sugar intake to the pathogenesis of type 2 diabetes has not been settled in the context of primary prevention because of limited prospective data.
The Women's Health Study is a randomized controlled trial of aspirin and vitamin E in the prevention of cardiovascular disease and cancer. A validated semiquantitative food frequency questionnaire was completed by 39,345 women aged 45 years and older. The main outcome was the incidence of type 2 diabetes. The predictor was sugar intake, including sucrose, glucose, fructose, and lactose. Using Cox proportional hazard models, multivariate RRs of type 2 diabetes for increasing quintiles of sugar intake compared with the lowest quintile were estimated.
Compared with the lowest quintile of sugar intake, the RRs and 95% CIs for the highest quintiles were 0.84 (0.67-1.04) for sucrose, 0.96 (0.78-1.19) for fructose, 1.04 (0.85-1.28) for glucose, and 0.99 (0.80-1.22) for lactose, after adjustment for known risk factors for type 2 diabetes. Similar findings of no association were obtained in subgroup analyses stratified by BMI.
Intake of sugars does not appear to play a deleterious role in primary prevention of type 2 diabetes. These prospective data support the recent American Diabetes Association's guideline that a moderate amount of sugar can be incorporated in a healthy diet.
The long-term impact of dietary carbohydrate type, in particular sucrose, on insulin resistance and the development of diabetes and atherosclerosis is not established. Current guidelines for the healthy population advise restriction of sucrose intake. We investigated the effect of high- versus low-sucrose diet (25 vs. 10%, respectively, of total energy intake) in 13 healthy subjects aged 33 +/- 3 years (mean +/- SE), BMI 26.6 +/- 0.9 kg/m(2), in a randomized crossover design with sequential 6-week dietary interventions separated by a 4-week washout. Weight maintenance, eucaloric diets with identical macronutrient profiles and fiber content were designed. All food was weighed and distributed. Insulin action was assessed using a two-step euglycemic clamp; glycemic profiles were assessed by the continuous glucose monitoring system and vascular compliance by pulse-wave analysis. There was no change in weight across the study. Peripheral glucose uptake and suppression of endogenous glucose production were similar after each diet. Glycemic profiles and measures of vascular compliance did not change. A rise in total and LDL cholesterol was observed. In this study, a high-sucrose intake as part of an eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity, glycemic profiles, or measures of vascular compliance in healthy nondiabetic subjects.
High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated.
We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7).
IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy.
Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the high-fructose diet (r = -0.78, P < 0.05).
Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.
Fructose is an increasingly important commercial sweetener. However, some patients report abdominal symptoms after ingesting fructose-containing foods. The completeness of fructose absorption by the small intestine was assessed by breath hydrogen analysis in 16 healthy volunteers and incomplete absorption was defined as a peak rise in breath hydrogen of >20 parts per million. Fructose, 50 g as a 10% solution, was incompletely absorbed in 6 of 16 subjects (37.5%). Incomplete absorption was associated with symptoms of cramps or diarrhea, or both, in 5 of these 6 individuals. Incomplete absorption was both concentration- and dose-related. Three subjects incompletely absorbed 37.5 g of fructose. In comparison, all 15 subjects who were studied after ingestion of sucrose, 50 g as a 10% solution, completely absorbed this sugar load. Incomplete absorption of fructose should be considered as a possible cause of gastrointestinal symptoms.
Twelve carbohydrate-sensitive men selected due to their abnormally high insulin responses to a sucrose load and 12 men with normal insulin responses were fed diets containing 0, 7.5, and 15% fructose for 5 wk each in a cross-over design. The diets contained 43% total carbohydrate, 42% fat, and 15% protein. Initial fasting total cholesterol and low-density lipoprotein cholesterol were higher in the hyperinsulinemic men than in the controls. Diastolic blood pressure was not affected by diet, but systolic blood pressure was slightly higher after the men consumed the 0% fructose diet. Free fatty acids were not different. Total plasma cholesterol and low-density lipoprotein cholesterol were higher after the men consumed 7.5 and 15% fructose than when they consumed the 0% fructose diet. Plasma triglyceride increased significantly as fructose in the diets of the hyperinsulinemics increased, but was not affected in the controls. These changes in blood lipids are associated with heart disease.
... 8. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar - sweetened drinks and childhood obesity : a prospective, observational analysis. Lancet. 2001;357:505-508.pmid:11229668. ...
Glucose is a major source of energy for cell. In the basal state, the liver is the only tissue which produces glucose. The hepatic glucose production is regulated by glycaemia, insulin and glucagon levels. The plasma glucose level is maintained constant via an utilization of glucose by the insulin - and non-insulin - dependent tissues which equal to the hepatic glucose production. In the post-prandial state, plasma glucose level increases because of a plasma glucose appearance superior to glucose uptake by tissues. Following carbohydrate ingestion, the glucose which appears in plasma is the sum of the appearance of glucose from ingested carbohydrates and of the endogenous glucose production. The rise in plasma glucose level in response to carbohydrate ingestion is limited by the increase in glucose uptake and the inhibition of endogenous glucose production in response to hyperglycaemia and hyperinsulinaemia. Glycaemic response is also dependent on the nature of carbohydrate and on its mode of administration.
The small intestine can be described as an “active interface” between the external environment and the blood and lymph that distribute the absorbed materials for the metabolic needs of the body. The activity of the interface is created by the intestine’s lining of epithelial cells whose three major functions are digestion, absorption and secretion. The population is ever-changing, being constantly renewed by cells dividing in the intestinal crypts and replacing those enterocytes lost into the lumen of the bowel from the extrusion zone at the tips of the villi [1]. In most mammals the duration of the enterocyte’s life is about 48 hours, and it has been colourfully described as a “short life but a merry one”. The intestinal epithelium is truly an active interface for it can respond to the demands placed upon it by adapting its structure and function. Changes in the amount and type of food entering the tract can induce adaptations in its function. These occur by three basic mechanisms:
1.
Changes in the number of functional enterocytes.
2.
Changes in the carrier, enzymatic or metabolic processes of the enterocytes.
3.
Changes in the maturation of function in the enterocytes as they migrate up from the crypts to the extrusion zone at the villus tip.
To learn more about the metabolic effects of dietary fructose and sucrose, 12 type I and 12 type II diabetic subjects were fed three isocaloric (or isoenergic) diets for eight days each according to a randomized, crossover design. The three diets provided, respectively, 21% of the energy as fructose, 23% of the energy as sucrose, and almost all carbohydrate energy as starch. The fructose diet resulted in significantly lower one- and two-hour postprandial plasma glucose levels, overall mean plasma glucose levels, and urinary glucose excretion in both type I and type II subjects than did the starch diet. There were no significant differences between the sucrose and starch diets in any of the measures of glycemic control in either subject group. The fructose and sucrose diets did not significantly increase serum triglyceride values when compared with the starch diet, but both increased postprandial serum lactate levels. We conclude that short-term replacement of other carbohydrate sources in the diabetic diet with fructose will improve glycemic control, whereas replacement with sucrose will not aggravate glycemic control.(JAMA 1986;256:3241-3246)
Objective.
—To examine prospectively the relationship between glycemic diets, low fiber intake, and risk of non—insulin-dependent diabetes mellitus.Desing.
—Cohort study.Setting.
—In 1986, a total of 65173 US women 40 to 65 years of age and free from diagnosed cardiovascular disease, cancer, and diabetes completed a detailed dietary questionnaire from which we calculated usual intake of total and specific sources of dietary fiber, dietary glycemic index, and glycemic load.Main Outcome Measure.
—Non—insulin-dependent diabetes mellitus.Results.
—During 6 years of follow-up, 915 incident cases of diabetes were documented. The dietary glycemic index was positively associated with risk of diabetes after adjustment for age, body mass index, smoking, physical activity, family history of diabetes, alcohol and cereal fiber intake, and total energy intake. Comparing the highest with the lowest quintile, the relative risk (RR) of diabetes was 1.37 (95% confidence interval [CI], 1.09-1.71, Ptrend=.005). The glycemic load (an indicator of a global dietary insulin demand) was also positively associated with diabetes (RR=1.47; 95% CI, 1.16-1.86, Ptrend=.003). Cereal fiber intake was inversely associated with risk of diabetes when comparing the extreme quintiles (RR=0.72,95% CI, 0.58-0.90, Ptrend=.001). The combination of a high glycemic load and a low cereal fiber intake further increased the risk of diabetes (RR=2.50, 95% CI, 1.14-5.51) when compared with a low glycemic load and high cereal fiber intake.Conclusions.
—Our results support the hypothesis that diets with a high glycemic load and a low cereal fiber content increase risk of diabetes in women. Further, they suggest that grains should be consumed in a minimally refined form to reduce the incidence of diabetes.
Ten men and nine women ages 35 to 55 consumed two diets for 6 weeks each in a cross-over design. The diets were composed of identical natural foods and 30% of the calories as either sucrose or wheat starch. Carbohydrate, fat, and protein supplied 43, 42, and 15% of the calories, respectively. Of the calories 10% was eaten at breakfast (7:00 to 8:30 AM) and 90% at dinner (4:30 to 6:30 PM). Inital body weights were essentially maintained. Fasting serum insulin and glucose levels were significantly higher with the sucrose than with the starch diet. The insulin response and the insulin:glucose ratios after a sucrose load (2 g/kg body weight) were greater after the subjects consumed the sucrose diet. Sucrose feeding produced increases in fasting serum insulin, the insulin:glucose ratio and the insulin response to a sucrose load that were of greater magnitude in a subgroup of nine subjects classified as potentially carbohydrate-sensitive than in normal subjects. Glucose response to a sucrose load and fasting serum glucagon did not differ significantly with diet. Fasting insulin and glucose showed significant increases as a function of time on diet. These results indicate that sucrose feeding produces undersirable changes in several of the parameters associated with glucose tolerance.
The human colon carcinoma cell line Caco-2 was used as an enterocyte model to study the expression of the facilitative glucose transporters GLUT-1 and GLUT-2, and of the putative hexose transporter GLUT-5, which are expressed specifically in the gut. Northern blots indicate that Caco-2 cells express GLUT-1 and GLUT-5 mRNAs but not the mRNA coding for the basolateral glucose transporter GLUT-2. The level of GLUT-5 mRNA is growth dependent, being detectable only in postconfluent differentiated cells. In addition, the expression of GLUT-5 increases with the number of cell passages and is approximately 10 times higher in later passages (passage 184) than in early ones (passage 26). With the use of polyclonal antibodies directed against the COOH-terminus of GLUT-5, indirect immunofluorescence and Western blotting indicate that GLUT-5 is mainly localized to the brush border of Caco-2 cells. GLUT-5 is also found to be associated with the brush border of epithelial cells from fetal and normal adult human small intestine, but is absent from the colon.
The use of 13C labelled glucose in human metabolic studies has been limited by the high cost of the tracer and the problems of measuring low 13C isotopic abundance in plasma glucose. In the present work we describe a new gas chromatograph-isotope ratio mass spectrometer allowing the measurement of a 0.001 atom % increase in 13C abundance over baseline, on a nanomole glucose sample. Studies were performed in rats and in human subjects. The rate of glucose appearance in 24 h fasted rats using D-[1-13C] glucose as tracer and analysed by this new method was found to be 10.4 +/- 0.7 mg.kg-1.min-1, a value 21% lower than that found using D-[6,6-2H2] glucose as tracer (13.1 +/- 1.1 mg.kg-1.min-1) analysed by classic gas chromatography-mass spectrometry. The new method was also used to trace, in combination with D-[6,6 2H2] glucose, the metabolic fate in human subjects of two oral glucose loads (0.5 g.kg.-1,1 g.kg.-1) labelled with 0.1% D-[U-13C] glucose. During the six hours following the glucose load, it was found that total glucose appearance was 0.97 +/- 0.04 g.kg.-1 and 1.2 +/- 0.04 g.kg.-1, exogenous glucose appearance was 0.51 +/- 0.02 g.kg.-1 and 0.84 +/- 0.04 g.kg.-1, endogenous glucose production was 0.44 +/- 0.04 g.kg.-1 and 0.35 +/- 0.06 g.kg.-1 after the 0.5 and 1 g.kg.-1 load respectively. These values are similar to those reported using glucose labelled with radioactive isotopes.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of dietary fructose on glycemic control in subjects with diabetes mellitus is controversial. Therefore our aim was to conduct a long-term study to examine the effects of dietary fructose on glucose tolerance and insulin sensitivity and to delineate the mechanisms for the effects observed. Six subjects with non-insulin-dependent diabetes mellitus (NIDDM) who were being treated by diet alone consumed 13% of their calories as fructose incorporated into mixed meals in place of sucrose for 3 months as inpatients on a metabolic ward. The following parameters were measured: (1) weekly fasting plasma-glucose concentrations, (2) postprandial serum glucose and insulin levels after four sugar tolerance tests, (3) basal hepatic glucose production, and (4) hepatic and whole-body insulin sensitivity determined during a hyperinsulinemic, euglycemic clamp. When modest amounts of fructose were substituted for sucrose in the diet for 3 months, basal hepatic glucose output remained unchanged (12.84 +/- 1.83 nmol/kg/min v 12.51 +/- 2.00 nmol/kg/min) as did hepatic insulin sensitivity (92% +/- 4% v 93% +/- 4% suppression) and peripheral glucose disposal (22.52 +/- 4.56 nmol/kg/min v 25.80 +/- 9.45 nmol/kg/min) to a 860 pmol/m2/min insulin infusion at euglycemia (4.8 mmol/L). Fructose feeding also did not alter fasting plasma-glucose concentrations or postprandial plasma glucose and insulin responses to oral glucose or fructose loads or to mixed meals containing either sucrose or fructose. In conclusion, substitution of physiologic amounts of sucrose by fructose for prolonged periods is unlikely to have adverse effects on glucose metabolism in diabetic subjects who are being treated with diet alone.
This study examined the rates of gastric emptying for water and 13 different carbohydrate-containing solutions in seven subjects, using conventional gastric intubation techniques. The rates of gastric emptying for water and a 10% glucose-polymer solution were also measured during 90 min of treadmill running at 75% of each subject's maximum oxygen consumption (VO2max). At rest, 15% glucose-polymer (P) and fructose (F) solutions emptied more rapidly from the stomach and provided a faster rate of carbohydrate delivery than did a 15% glucose (G) solution (p less than 0.05). The G solutions showed a constant energy delivery rate of 3.3 kcal.min-1; energy delivery from P and F solutions rose with increasing solution concentrations. The osmolality of the gastric aspirate predicted the rate of gastric emptying for all solutions (p less than 0.05) but overestimated rates of emptying for 10% and 15% P solutions and underestimated emptying rates for 10% and 15% F solutions. Exercise at 75% VO2max decreased the rate of gastric emptying of water but not of 10% P solutions. Thus the different rates of gastric emptying for different carbohydrate-containing solutions were not entirely explained by differences in osmolality. Furthermore, exercise may have different effects on the gastric emptying rates of water and carbohydrate solutions.
We studied the metabolic effects of 2-wk fructose feeding as the sweetener in the diet of seven non-insulin-dependent diabetic individuals. The data demonstrated reduced postprandial hyperglycemia to an oral glucose challenge after 14 days without a significant difference in insulin response. There was no change in the markedly blunted glucose response to a fructose challenge but a significantly lower insulin response (area under the 3-h curve) was observed after 14 days of fructose feeding. There was reduced postprandial hyperglycemia after 14 days of fructose feeding with test meals as compared with baseline, without significant differences in insulin response. We also found no significant difference in free fatty acids, cholesterol, high-density lipoprotein (HDL) cholesterol, pyruvate, lactate, or uric acid after fructose feedings. There was a 13% increase in triglyceride levels after 14 days in 5 subjects with initial fasting hypertriglyceridemia (greater than 150 mg/dl). Insulin receptor binding to isolated adipocytes did not change after 14 days of fructose feeding.
The effects of regularly eating sucrose were studied in 23 diabetic patients, 12 Type 1 (insulin-dependent) and 11 Type 2 (non-insulin-dependent), with differing degrees of glycaemic control. Two diets, each lasting 6 weeks, were compared in a randomised cross-over study. Both diets were high in fibre and low in fat. In one diet 45 g of complex carbohydrate was replaced by 45 g of sucrose taken at mealtimes. There were no significant biochemical differences between the two diets in either Type 1 or Type 2 patients. In Type 1 patients the mean (+/- SEM) fasting plasma glucose was 10.5 (1.8)mmol/l on the control diet and 10.3 (1.5) mmol/l on sucrose. In Type 2 patients the levels were 9.1 (0.8) mmol/l and 8.9 (0.8) mmol/l respectively. Glycosylated haemoglobin for the Type 1 patients was 9.9% on control and 10.3% on sucrose; for Type 2 patients the figures were 9.3% and 9.0% respectively. There were no differences in mean daily plasma glucose levels or diurnal glucose profiles. Cholesterol (total and in lipoprotein fractions) was unchanged, as were diurnal triglyceride profiles and plasma insulin profiles in the Type 2 patients. There were no changes in medication or body weight. We conclude that a moderate amount of sucrose taken daily at mealtimes does not cause deterioration in metabolic control in diabetic patients following a high fibre/low fat diet.
To learn more about the metabolic effects of dietary fructose and sucrose, 12 type I and 12 type II diabetic subjects were fed three isocaloric (or isoenergic) diets for eight days each according to a randomized, crossover design. The three diets provided, respectively, 21% of the energy as fructose, 23% of the energy as sucrose, and almost all carbohydrate energy as starch. The fructose diet resulted in significantly lower one- and two-hour postprandial plasma glucose levels, overall mean plasma glucose levels, and urinary glucose excretion in both type I and type II subjects than did the starch diet. There were no significant differences between the sucrose and starch diets in any of the measures of glycemic control in either subject group. The fructose and sucrose diets did not significantly increase serum triglyceride values when compared with the starch diet, but both increased postprandial serum lactate levels. We conclude that short-term replacement of other carbohydrate sources in the diabetic diet with fructose will improve glycemic control, whereas replacement with sucrose will not aggravate glycemic control.
The intravenous injection of fructose (200 or 400 mg) into the anesthetized rat leads to a prompt increase in the hepatic α-glycerophosphate concentration. However, this increase is transient since the α-glycerophosphate concentration returns to control levels within 20 min after fructose injection. Analysis of the plasma fructose concentration at this time shows that the fall in the hepatic α-glycerophosphate concentration cannot be due to a lack of substrate for fructokinase (EC 2.7.1.3). The changes in the hepatic pyruvate concentration after intravenous fructose mirrored those for α-glycerophosphate.In comparison to fructose, glucose injection did not lead to an early increase in the hepatic α-glycerophosphate concentration. 20 min after intravenous glucose, the hepatic α-glycerophosphate concentration was nearly 2-fold greater than the control values.The data indicate that the effects of fructose on hepatic fatty acid metabolism cannot be related to sustained increases in hepatic α-glycerophosphate concentration. They also demonstrate that under certain conditions, the hepatic α-glycerophosphate concentration may be greater after glucose than after fructose administration.
The livers of rats given large injections of fructose or dihydroxyacetone were analyzed for glucose, glycogen, and 14 related metabolites. Dihydroxyacetone produced a large increase in glycogen and a modest increase in glucose and glucose-6-P. Fructose produced no increase in glycogen but a large increase in glucose and glucose-6-P. Changes in intermediates suggest in both cases diversion of part of the injected material into the Embden-Meyerhof pathway. Fructose caused a profound drop in ATP, UTP and UDPG. The fall in ATP is attributed to sequestration of phosphate into fructose-1-P, which increased to 18 mmole/kg. The decrease in ATP is believed to lead in turn to the fall in UTP and UDPG and the failure to deposit glycogen.
Twelve men with abnormally high insulin responses to a sucrose load and 12 normal men were fed diets containing 0, 7.5, or 15% of the calories as fructose for 5 weeks each. The diets contained approximately 43% of the calories as total carbohydrate, 42% as fat and 15% as protein. Mean insulin responses of the hyperinsulinemic men were initially 235% of control responses. Plasma glucose concentrations 1 hour after the sucrose load were significantly higher in hyperinsulinemic men than in controls. There were no initial differences between the two groups in glucagon or gastric inhibitory polypeptide (GIP) responses. Consumption of 7.5 and 15% Fructose diets increased fasting plasma glucose and GIP responses in both groups. Consumption of the 15% fructose diet resulted in significantly higher insulin and glucose responses than consumption of the other two diets. These results indicate that moderate levels of dietary fructose can produce undesirable changes in glucose metabolism of both normal and hyperinsulinemic men.
Isomalt (Palatinit) an equimolar mixture of alpha-D-glucopyranosido-1,6-sorbitol and alpha-D-glucopyranosido-1,6-mannitol, was compared to sucrose in a prospective double-blind controlled crossover study. The acute effects of oral ingestion of 30-g loads of isomalt or sucrose on plasma glucose, insulin, free fatty acids (FFA), lactic acid, and carbohydrate (CHO) and lipid oxidation were studied over six hours by means of continuous indirect calorimetry in ten healthy normal-weight subjects. Unlike sucrose, whose ingestion was followed by significant changes in plasma glucose, insulin, and lactic acid during the first 60 minutes of the test, no significant changes in these parameters were observed following the administration of isomalt. The increase in CHO oxidation occurring between 30 and 150 minutes was significantly lower (P less than 0.01) following isomalt than after sucrose. Conversely, the decrease in lipid oxidation was significantly less (P less than 0.01) after isomalt in comparison to sucrose. It is concluded that the rise in CHO oxidation and in plasma glucose and insulin levels is markedly reduced when sucrose is replaced by an equal weight of isomalt. In contrast to other sugar substitutes, no increase in plasma lactic acid was observed after isomalt administration.
Twelve carbohydrate-sensitive men selected due to their abnormally high insulin responses to a sucrose load and 12 men with normal insulin responses were fed diets containing 0, 7.5, and 15% fructose for 5 wk each in a cross-over design. The diets contained 43% total carbohydrate, 42% fat, and 15% protein. Initial fasting total cholesterol and low-density lipoprotein cholesterol were higher in the hyperinsulinemic men than in the controls. Diastolic blood pressure was not affected by diet, but systolic blood pressure was slightly higher after the men consumed the 0% fructose diet. Free fatty acids were not different. Total plasma cholesterol and low-density lipoprotein cholesterol were higher after the men consumed 7.5 and 15% fructose than when they consumed the 0% fructose diet. Plasma triglyceride increased significantly as fructose in the diets of the hyperinsulinemics increased, but was not affected in the controls. These changes in blood lipids are associated with heart disease.
Fructose is an increasingly important commercial sweetener. However, some patients report abdominal symptoms after ingesting fructose-containing foods. The completeness of fructose absorption by the small intestine was assessed by breath hydrogen analysis in 16 healthy volunteers and incomplete absorption was defined as a peak rise in breath hydrogen of greater than 20 parts per million. Fructose, 50 g as a 10% solution, was incompletely absorbed in 6 of 16 subjects (37.5%). Incomplete absorption was associated with symptoms of cramps or diarrhea, or both in 5 of these 6 individuals. Incomplete absorption was both concentration- and dose-related. Three subjects incompletely absorbed 37.5 g of fructose. In comparison, all 15 subjects who were studied after ingestion of sucrose, 50 g and a 10% solution, completely absorbed this sugar load. Incomplete absorption of fructose should be considered as a possible case of gastrointestinal symptoms.
Twenty-four adult men and women, classified as carbohydrate-sensitive on the basis of an exaggerated insulin response to a sucrose load, consumed diets containing 5, 18, and 33% of calories as sucrose for 6 wk each in a cross-over design. The diets contained identical natural and processed foods except for a patty containing 2, 15, or 30% of the calories as sucrose at the expense of wheat starch. Carbohydrate, fat, and protein provided 44, 42, and 14% of the calories, respectively. Of total calories, 25% were consumed at breakfast and 75% at dinner. Initial body weights of the subjects were essentially maintained. Fasting serum insulin levels increased with the sucrose content of the diet and were significantly higher in men than in women. Mean fasting glucose was significantly higher on either 18 or 33% sucrose than on 5% sucrose. The sucrose content of the diet did not affect fasting serum glucagon. When compared to the insulin response to a sucrose load (2 g/kg body weight) after consuming the 5% sucrose diet, serum insulin was significantly higher at 1 h after the 18% sucrose diet and at 0.5, 1, 2, and 3 h after the 33% sucrose diet. Except after 2 h, the glucose response was significantly greater after the 18 and 33% sucrose diets than after the 5% sucrose diet. These results indicate that sucrose intake by carbohydrate-sensitive individuals, even at levels approximating the average United States intake, can produce undesirable changes in several parameters associated with glucose tolerance.
To assess in diabetic subjects the effects of dietary sucrose on glycemia and lipemia.
Twelve type II diabetic subjects consumed, in random order, two isocaloric, 55% carbohydrate study diets for 28 days. In one diet, 19% of energy was derived from sucrose. In the other diet, < 3% of energy was derived from sucrose, and carbohydrate energy came primarily from starch. Both study diets were composed of common foods. All meals were prepared in a metabolic kitchen where foods were weighed during meal preparation.
No significant differences were noted between the study diets at any time point in mean plasma glucose. At day 28, mean plasma glucose values for the sucrose diet were 9.6 +/- 0.5 mM and for the starch diet were 9.4 +/- 0.6 mM (P = 0.63). Also, no significant differences were observed between the study diets in urine glucose, fasting serum total, HDL, or LDL cholesterol; fasting serum TG; or peak postprandial serum TG.
A high sucrose diet did not adversely affect glycemia or lipemia in type II diabetic subjects.
The effect of dietary fructose (20% of carbohydrate calories, 45-65 g day-1 for 4 weeks) on glycaemic control, serum lipid, lipoprotein and apoprotein A-I and A-II concentrations and on insulin sensitivity was studied in 10 type 2 diabetic patients. The study was done in a randomized, double-blind fashion with crystalline fructose or placebo administered evenly during 4 meals or snacks per day. The patients were hospitalized throughout the study periods. The fasting plasma glucose concentration decreased during the fructose (from 10.7 +/- 1.4 mmol l-1 to 8.0 +/- 0.8 mmol l-1, P < 0.02) and the control diet (from 10.1 +/- 0.9 mmol l-1 to 8.0 +/- 0.7 mmol l-1, P < 0.05). The mean diurnal blood glucose concentration also fell both during the fructose (from 10.8 +/- 0.5 mmol l-1 to 8.4 +/- 0.3 mmol l-1, P < 0.001) and the control diet (from 10.3 +/- 0.3 mmol l-1 to 8.8 +/- 0.9 mmol l-1, P < 0.01). The HbA1 concentration improved (P < 0.02) only during the fructose diet. Insulin sensitivity increased by 34% (P < 0.05) during the fructose diet, but remained unchanged during the control period. Serum insulin, triglyceride, apoprotein A-I and A-II concentrations, body we