ArticleLiterature Review

Effects of Sucrose on Carbohydrate and Lipid Metabolism in NIDDM Patients

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Recently, there has been increasing interest toward the liberalization of sucrose in the diets of individuals with non-insulin-dependent diabetes mellitus (NIDDM). However, there is evidence from several well-controlled prospective studies demonstrating that the consumption of moderate amounts of sucrose may result in hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and reduced high-density lipoprotein cholesterol concentrations. The fact that not all studies demonstrate these deleterious effects does not negate the positive data. The magnitude of the deleterious effects will probably vary with individual patients, baseline status, and amount of sucrose. Because these metabolic abnormalities are most disturbed in diabetes and are associated with increased risk of coronary artery disease, it would seem reasonable to continue to advise patients with NIDDM to limit sucrose consumption, at least until available data would allow us to predict in which individuals and at what level of sucrose consumption these adverse metabolic effects would not be present.

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... The rates of severe hypoglycemia and hyperglycemia were alarmingly high in the Epidemiology of Diabetes and Ramadan study, a population-based large epidemiological study that spanned 13 countries with sizeable Muslim populations (3). Such a high rate of fasting-related morbidity was reported earlier in a small study by Uysal et al. (4). Education of patients is the cornerstone of safe fasting, which is needed on both an individual and large-scale level, and this is the responsibility of diabetes care team members. ...
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Al-Arouj et al. (1) have made recommendations for fasting during the holy month of Ramadan for Muslim diabetic patients. The recommendations were drafted by an expert panel of diabetologists from around the globe, and it represents a landmark for practicing clinicians who look after diabetic Muslims. The recommendations were based on expert opinion rather than evidence-based scientific research, which, as the panel pointed out, is lacking in this area. These provisional recommendations await well-designed research aimed specifically at seeing whether fasting is beneficial or harmful to patients with type 1 diabetes. Type 1 diabetic patients are often advised not to fast by physicians. The nature of …
... Diets with high carbohydrates (e.g. sucrose) have been shown to accentuate metabolic abnormalities, including hypertriglyceridemia [74,164]. There is a well-established carbohydrate-induced stimulation of plasma TG (both in VLDL and CM) in the fasting state as well as an effect of carbohydrate feeding on postprandial lipemia, even after a single meal [reviewed in [142]]. ...
Chylomicrons (CM), secreted by the intestine in response to fat ingestion and to a lesser extent during the postabsorptive state (lipid poor CM), are the major vehicles whereby ingested lipids are transported to and partitioned in energy-storing and energy-utilizing tissues of the body. CM contribute significantly, although not exclusively, to postprandial lipemia. Intestinal CM production is upregulated in humans under conditions of insulin resistance and CM overproduction in such conditions contributes to the highly prevalent dyslipidemia of these conditions. In addition, CM remnants possess direct atherogenic properties. CM assembly and secretion is regulated by many factors apart from ingested fat (the primary stimulus for their secretion), including a number of nutritional, hormonal, metabolic and genetic factors. Understanding the mechanisms that regulate CM production in health and disease may lead to treatments and prevention of atherosclerosis and cardiovascular disease. This review aims to summarize current understanding of CM production in humans. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease.
... Dietary practice plays a central role in glycemic control (16). The use of sucrose-sweetened beverages has been shown to be associated with hyperglycemia and the development of insulin resistance or type 2 diabetes (17)(18)(19)(20). Whether the latter is attributed to the proposed acute effects of sucrose-sweetened beverage consumption (eg, induction of postprandial hyperglycemia and the stimulation of excess energy intake and subsequent development of obesity) remains unresolved. ...
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Hyperglycemia forms a direct and independent risk factor for the development of cardiovascular comorbidities in type 2 diabetes. Consumption of sucrose-sweetened soft drinks might further increase the prevalence of hyperglycemic episodes. The objective was to assess glycemic control in type 2 diabetic subjects and healthy lean and obese control subjects under strict dietary standardization but otherwise free-living conditions, with and without the consumption of soft drinks. Obese type 2 diabetic men (n = 11) and lean (n = 10) and obese (n = 10) normoglycemic male control subjects participated in a randomized crossover study. The subjects were provided with a standardized diet in 2 periods, during which they consumed 250 mL water with or without (control) sucrose (37.5 g) 2 h after breakfast and lunch. Blood glucose concentrations were assessed by continuous glucose monitoring. In the type 2 diabetic subjects, the mean 24-h glucose concentrations were significantly elevated (9.1 +/- 0.6 mmol/L), and hyperglycemia (glucose >10 mmol/L) was evident over 33 +/- 8% (8 +/- 2 h) of a 24-h period (P < 0.01). Hyperglycemia was rarely present in the normoglycemic lean and obese control subjects (5 +/- 2%/24 h for both). Consumption of 75 g sucrose, equivalent to 2 cans of a soft drink, did not further augment the prevalence of hyperglycemia throughout the day in any group. Type 2 diabetic subjects taking oral blood glucose-lowering medication experience hyperglycemia during most of the daytime. Moderate consumption of sucrose-sweetened beverages does not further increase the prevalence of hyperglycemia in type 2 diabetic subjects or in normoglycemic lean or obese men.
... Regarding carbohydrate, the average percentage carbohydrate of the caloric intake was modified from 42.2 ± 0.8 to 44.0 ± 0.9% in group A and from 40.7 ± 0.8 to 40.7 ± 0.7% in group B. Diabeto tolerates 45-55% carbohydrate (23)(24)(25)(26)(27)(28)(29)(30). For patients whose initial carbohydrate intake was insufficient (<45%), the percentage increased Regarding fats, the average percentage fat of the caloric intake was modified from 38.3 ± 1 . ...
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To evaluate Diabeto, a computer-assisted diet education system. One hundred five patients with insulin-dependent diabetes mellitus (IDDM) or non-insulin-dependent diabetes mellitus (NIDDM) were divided into two randomized groups to participate in the evaluation of Diabeto. With free access through Minitel, the French public videotex network, Diabeto helps diabetic patients self-monitor their diets and balance their meals with personalized counseling. During the first 6-mo study, group A (54 patients) used Diabeto, whereas group B (51 patients) were control subjects. For the second 6-mo study, group B used the system. Evaluation was based on patients' dietetic knowledge, dietary habits, and metabolic balance. Diabeto led to a significant improvement of dietetic, knowledge in group A (P less than 0.0005) and also to improved dietary habits; decreased caloric intake in patients initially overeating (P less than 0.05), increase of dietary carbohydrate from 39.7 +/- 0.7 to 42.9 +/- 0.9% in patients with an initial intake less than 45% carbohydrate, and decrease of fat intake from 41.9 +/- 0.9 to 37.4 +/- 1.1% in patients with an initial intake of greater than 35% fat (P less than 0.0005). In the second study, in addition to similar improvements to those observed in the first study, HbA1 decreased from 11.0 +/- 0.4 to 9.9 +/- 0.4% (P less than 0.005) and fructosamine from 5.00 +/- 0.17 to 4.57 +/- 0.17% (P less than 0.001). Diabeto appears to be an effective therapeutic tool in the control of metabolic diseases.
... In general, individuals with type II diabetes are overweight and need overall calorie restriction rather than permission to eat desserts that would probably increase their daily calorie intake. Two excellent reviews have recently been published that discuss the controversies in this area (12,22). On the other hand, children and young adults with type I diabetes do not usually require calorie restriction. ...
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Traditional dietary advice given to people with diabetes includes eliminating simple sugars (primarily sucrose) from the diet. Many people have difficulty following this recommendation. Because patients with type I (insulin-dependent) diabetes do not need overall calorie restriction, there is no caloric reason to restrict sucrose. In this study, we looked at the effect of the isocaloric substitution of a piece of chocolate cake for a baked potato in a mixed meal to determine whether this would increase the blood glucose in patients with type I diabetes. The glucose response to a cake-added meal was significantly greater than to a standard meal. The glucose response was no different between a cake-substitution meal and a standard meal. The reproducibility studies showed no difference between repeated standard meals. The urinary glucose excretion was significantly greater after a cake-added meal but was no different with the other pairs. There were no significant differences in the counterregulatory hormone responses at baseline between any of the paired studies. In conclusion, patients with type I diabetes may substitute a sucrose-containing dessert for another carbohydrate in their diet without compromising their postprandial glucose response. These data suggest that a dessert exchange may be helpful and not harmful in the management of diabetic patients. There is an inherent variability (at least 16%) in an insulin-requiring patient's response to a meal, making self-monitoring of blood glucose and adjustment of insulin doses necessary to achieve near euglycemia.
... There have been concerns that high carbohydrate intakes at the expense of fat, particularly monounsaturated fat (Coulston et al, 1989;Mensink and Katan, 1987;Garg et al, 1994) could result in a rise in triglycerides and very-lowdensity lipoproteins and a suppression of HDL levels, which could translate into a higher risk of heart disease (Gordon et al, 1989;Stampfer et al, 1996;Vega & Grundy, 1996;Hokanson & Austin, 1996). However, not all carbohydrate-rich diets may produce the same effects on HDL levels, as low-GI diets may confer a more favorable lipid profile compared with high-GI diets. ...
Aim: The intent of this review is to critically analyze the scientific evidence on the role of the glycemic index in chronic Western disease and to discuss the utility of the glycemic index in the prevention and management of these disease states. Background: The glycemic index ranks foods based on their postprandial blood glucose response. Hyperinsulinemia and insulin resistance, as well as their determinants (eg high energy intake, obesity, lack of physical activity) have been implicated in the etiology of diabetes, coronary heart disease and cancer. Recently, among dietary factors, carbohydrates have attracted much attention as a significant culprit, however, different types of carbohydrate produce varying glycemic and insulinemic responses. Low glycemic index foods, characterized by slowly absorbed carbohydrates, have been shown in some studies to produce beneficial effects on glucose control, hyperinsulinemia, insulin resistance, blood lipids and satiety. Method: Studies on the short and long-term metabolic effects of diets with different glycemic indices will be presented and discussed. The review will focus primarily on clinical and epidemiological data, and will briefly discuss in vitro and animal studies related to possible mechanisms by which the glycemic index may influence chronic disease.
... The rates of severe hypoglycemia and hyperglycemia were alarmingly high in the Epidemiology of Diabetes and Ramadan study, a population-based large epidemiological study that spanned 13 countries with sizeable Muslim populations (3). Such a high rate of fasting-related morbidity was reported earlier in a small study by Uysal et al. (4). Education of patients is the cornerstone of safe fasting, which is needed on both an individual and large-scale level, and this is the responsibility of diabetes care team members. ...
Many experimental studies on sugar (sucrose) omitted its form of ingestion. Often their findings were mutually incompatible. A comparison of the results of the few studies that administered sugar in a single specified form suggests that the metabolic effects of sugar depend on its form of ingestion, because even 80% of calories as diluted sugar proved harmless, but only 30% of calories as undiluted sugar proved harmful. These opposite effects of sugar can be explained by the published hypothesis that evolution adapted genetically our ancestors to cope with sugar only in diluted forms, because prehistorically diluted sugar was available abundantly in fresh fruits, but undiluted sugar was inexistent. The purpose of this review, based mainly on the evolutionary interpretation of published data of physiology, is to encourage researchers to perform an unprecedented experimental study to compare the metabolic effects of diluted sugar with the effects of undiluted sugar. The data of physiology analyzed in this review suggest that the absorption of diluted sugar within the caloric range of total sugars diluted in fresh fruits is slow and calorie-constant, thus preserving blood glucose homeostasis, whereas the absorption of concentrated sugar exceeding that caloric range is rapid, which can disrupt blood glucose homeostasis. Dietary salt, which was unknown to prehistoric humans, unnaturally accelerates the absorption of sugars. This can explain the harmful effects attributed to sugar-sweetened beverages per se, because these drinks are generally co-ingested with foods containing salt, which partly yet unavoidably passes into those beverages, thereby unhealthily accelerating their absorption.
It is only recently that man has been exposed to a significant intake of sweetness in the diet. The pattern of sweetener use is rapidly changing; use of sucrose from cane and beet is giving way to corn-derived syrups (which contain fructose as well as sucrose), new nutritive sweeteners such as sorbitol and xylitol, and a rapidly growing use of intense, non-nutritive (or artificial) sweeteners such as saccharin and aspartame. This chapter considers the metabolic fate of this variety of sweet-tasting dietary components, how they may affect health, and the problems they pose for individuals already suffering from certain metabolic diseases such as diabetes mellitus and phenylketonuria.
The dietary management of hyperlipoproteinaemia is one of the primary strategies in preventing coronary heart disease (CHD). The effect of reduced calory intake on fasting blood lipids and apolipoproteins by exchanging fat for carbohydrate and replacing saturated dietary fats with vegetable or marine oils are well-documented. The nutritional implications on postprandial triacylglycerolaemia have recently been reviewed (1) and the specific role of polyunsaturated fatty acids in lowering fasting plasma lipids and apolipoproteins has recently been reviewed by Lichtenstein (2). Considerably less is known about diet as a means of modulating postprandial lipoprotein metabolism, which to some extent depends on the fact that pertinent studies have used a variety of methods to provoke the system, ie the composition and size of test meals. As a further complication there is no consensus as to how quantification of postprandial lipids and apolipoproteins should be carried out (3). The present review deals with the effects of diet on postprandial lipaemia and its relevance for the development of CHD.
The pathophysiological bases and clinical implications of postprandial hyperlipidemia, i.e. the abnormal lipoprotein concentration and composition changes after a meal, are reviewed. Due to the heterogeneity of the lipoproteins involved, as well as methodological difficulties, the mechanisms behind these postprandial changes have not been clearly defined. While to date there are no prospective or intervention studies relating postprandial hyperlipidemia to cardiovascular events, the clinical relevance and the interest in the scientific community on this issue are anyhow very high. Much evidence, in fact, suggest that postprandial lipoproteins are atherogenic and are related to cardiovascular disease also independently of fasting lipid levels. The atherogenic mechanisms through which postprandial hyperlipidemia could act are discussed, as well as its relation with insulin resistance and related conditions, and the effects of diet, physical exercise and drugs on postprandial lipemia.
Diabetes mellitus is a risk factor for atherosclerotic vascular disease in women due to both an independent contribution of the diabetes and the associated dyslipidemia. This chapter discusses diabetes mellitus in general, with emphasis on these issues. Data are derived from studies in both men and women, but there is special emphasis on the impact in women.
As the population ages, we are faced with a marked rise in the number of frail elderly, many of who may require nutritional support. The provision of tube feeding in these patients has undergone major changes in the last few decades, particularly with the advent of percutaneous endoscopic gastrostomy as the preferred method for long-term feeding. A large number of formulae are now commercially available in order to supply the specific nutritional needs of patients. This review will present a comprehensive approach to the subject of enteral feeding in later life and will highlight some of the contentious ethical issues relating to this intervention.
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Any attempt to delete NIDDM as a major component of the diabetes mellitus syndrome is certain to meet major resistance. However, the purpose of this paper has been to review the evidence that suggests the term may be inappropriate. In future reviews of the classification of diabetes, this evidence will need to be seriously considered.
Obesity induced by long-term consumption of a fat-rich diet causes marked endothelial dysfunction. In this study we aimed to determine whether endothelial impairment is due to obesity or the diet per se. Wistar rats were fed either standard laboratory chow throughout (controls), or given a highly palatable diet (diet-fed) for 3 days, or fed the diet for 3 days and then returned to chow for 3 further days before sacrifice (diet-to-chow). Body weight, fat and gastrocnemius muscle mass, and plasma levels of glucose, insulin and leptin were all comparable between the three groups. Diet-fed rats had significantly raised plasma non-esterified fatty acids (NEFA; P=0.0005) and triglyceride levels (P=0.00001). The diet-to-chow group had intermediate plasma NEFA and triglyceride levels (significantly higher than in controls, P=0.019 and P=0.0035 for NEFA and triglycerides, respectively). There were no changes in noradrenaline and KCl responses in mesenteric arteries, whereas vasorelaxation to both carbamylcholine and sodium nitroprusside were significantly attenuated in the diet-fed group (by up to 18%; P=0.00001). Both these responses remained largely impaired in the diet-to-chow group. By contrast, histamine-induced vasorelaxation was comparable between all three groups. Thus, short-term feeding with a palatable diet induces marked endothelium-dependent and -independent arterial dysfunction. These effects occurred in the absence of obesity and largely persisted after removal of the palatable diet. Diet per se can have important detrimental effects on arterial function, which may be mediated by raised NEFA and/or triglyceride levels.
To test the hypothesis that the dietary intake and dietary composition of women with polycystic ovary syndrome (PCOS) is associated with indices of glycemic status. We hypothesized that women with PCOS would consume a diet higher in total energy, fat, and specific foods with a high glycemic index than would healthy, control-group women and that dietary composition would be associated with indices of insulin resistance and secretion among women with PCOS. Cohort study. Research center on a university campus. Thirty women with PCOS and 27 healthy, age-, race-, and body mass index (BMI)-matched control women. None. Nutrient intake data were collected from a food questionnaire and a 4-day food record. Fasting sera were analyzed for concentrations of insulin and glucose; estimates of insulin resistance were calculated. Consumption of total energy, macronutrients, micronutrients, and high glycemic index foods was similar between the groups. However, the PCOS group consumed significantly more white bread (7.9 +/- 4.4 vs. 5.5 +/- 2.9 servings over 4 days) and tended to consume more fried potatoes than did the control group (1.0 +/- 1.5 vs. 0.4 +/- 0.7 servings over 4 days). The PCOS group had a significantly greater fasting insulin concentration (22.5 +/- 14.9 vs. 15.1 +/- 8.3 muIU/mL) and a significantly lower glucose-to-insulin ratio (4.7 +/- 2.1 vs. 7.6 +/- 5.2) than the control group. Within the PCOS group, HOMA-IR and HOMA-%beta-cell function were significantly associated with BMI. The HOMA-IR, HOMA-%beta-cell, fasting insulin, and glucose-to-insulin ratio were not positively associated with measures of diet composition. Compared with matched control women, women with PCOS exhibited a dietary pattern that was marked by consumption of a greater amount of specific foods with a high glycemic index; however, diet composition was not associated with the greater fasting insulin concentration or with lower glucose-to-insulin ratio that was observed in the PCOS group.
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We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety. Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day. The dietary regimens continued for 1 week. Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose, insulin, and ketone bodies in the two groups studied. High-glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding (P less than 0.05) and insulin sensitivity (P less than 0.05). The changes in insulin binding and insulin sensitivity correlated linearly (r = 0.52, P less than 0.01). We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose.
For 6 weeks, 10 men and nine women aged 35 to 55 consumed each of two diets in a cross-over design. The diets were comprised of identical natural foods with 30% of the calories as either sucrose or cooked wheat starch. Carbohydrate, fat and protein supplied 43, 42, and 15% of the calories, respectively. Of the calories 10% were eaten at breakfast (7:00 to 8:30 AM) and 90% at dinner (4:30 to 6:30 PM). Initial body weights were essentially maintained. Total serum lipids, triglycerides, and total cholesterol levels were significantly higher when the subjects consumed the sucrose diet than when they consumed the starch diet. Increases associated with the sucrose diet were greatest for triglycerides (33.0%). In a subgroup of nine subjects with triglyceride levels above the normal range, sucrose feeding increased triglyceride levels 45.2%. Triglycerides and pre-beta lipoproteins were significantly higher in males than in females. Pre-beta lipoproteins were 32% higher when the subjects consumed sucrose than when they consumed starch. For alpha and beta lipoproteins, small, nonsignificant increases were associated with sucrose feeding. Serum free fatty acids were not affected by diet. These results indicate that the consumption of sucrose can increase blood lipids that are considered to be risk factors in heart disease and that males and carbohydrate-sensitive individuals may be more susceptible than others to the effects of sucrose.
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 relationship of glucose tolerance to the incidence of coronary heart disease (CHD) has been investigated in two cohorts of Finnish men: 3267 men ages 40--59 yr from the Social Insurance Institution's (SII) Coronary Heart Disease Study and 1059 men ages 30--59 yr from the Helsinki Policemen Study. The relationship of plasma insulin level to the incidence of CHD was also investigated in the Helsinki Policemen Study. An oral glucose lead of 60, 75, or 90 g according to body surface area was used in both studies. In the SII Study, plasma glucose was determined from venous blood samples taken 1 h after glucose load. In the Helsinki Policemen Study, blood glucose was determined from venous blood samples taken at 0, 1, and 2 h, and at a 5-yr reexamination, plasma insulin was measured during OGTT at 0, 1, 2 h. In the SII Study cohort, the 4-yr mortality from CHD and the 4-yr incidence of nonfatal myocardial infarction (MI) did not show a definite relationship to 1-h postload plasma glucose. In the Helsinki Policemen Study cohort, the 5-yr incidence of "hard criteria" CHD (CHD death and nonfatal MI) was significantly related to high 1-h postload blood glucose level but not to fasting or 2-h postload blood glucose levels. 10-yr mortality from CHD was significantly higher in the top quintile of fasting and 1- and 2-h postload blood glucose levels, as was the incidence of "hard criteria" CHD. However, in multivariate analyses including age, systolic blood pressure, plasma cholesterol, and smoking, the blood glucose variables showed no statistically significant independent contribution in predicted risk of CHD. Univariate analyses by quintiles of plasma insulin levels measured at the 5-yr reexamination showed that the incidence of "hard criteria" CHD during the subsequent 5 yr was significantly higher in the top quintiles of fasting and 1-h and 2-h postload plasma insulin than in the combined lower quintiles. Multivariate analyses showed that the value of high 1-h or 2-h postload plasma insulin level for predicting CHD risk was independent of other risk factors, including blood glucose levels during OGTT.
A 14-year follow-up of the Stockholm prospective study is reported. A number of 130 new myocardial infarctions (MI) were found in a prospective group of men (n = 3189) and another 46, i.e. a total of 176 MI, in the total group (n = 3486). Different types of multivariate statistical analyses show that age, blood pressure, smoking, fasting plasma concentrations of cholesterol and triglycerides, ESR and Hb were independent risk factors for MI, while the weight/height index was not. Elevated BP became an important risk factor only after the age of 50. When only age, BP, smoking and the two plasma lipids were entered into the logistic multivariate analysis, plasma triglycerides were more important as a risk factor than cholesterol. Quintile analysis showed that the rate of new MIs increased more with increasing triglyceride than increasing cholesterol levels. In the prospective group, the average rate of new MIs for men below 60 years was 32 per 1000. In the bottom and top quintile these rates were 16 and 65 for plasma triglycerides and 27 and 47 for cholesterol. When the men were divided into 4 groups with regard to both plasma lipids, the rate of new MIs increased successively from group to group along this chain: both lipids normal, only cholesterol high, only triglycerides high and both plasma lipids high.
Summary To ascertain whether the effects of diet on glucose tolerance and insulin sensitivity are mediated through changes of insulin receptors we have studied insulin binding to monocytes in 24 young volunteers (4 groups of 6) during 2 week periods of different dietary regimens. In group 1 and 2 the subjects had their usual diet plus 1000 kcal per day from sucrose or fat, respectively. Group 3 had an isocaloric diet with a low-sucrose content, while group 4 ate low-fat high carbohydrate diets. Before change of diet the total group of volunteers showed an inverse correlation between insulin binding and average daily sucrose intake (R = − 0.52, p
Normal subjects were given, on separate occasions, equivalent amounts of glucose, surcrose ("sugar''), and carbohydrates in the form of bread and starch. Neither the glucose, nor the insulin values showed any significant difference in these persons after they had been loaded with the various carbohydrates. The conclusion that can be drawn from this study is that neither the insulin demand nor the secretion rate of insulin are influenced by the type of carbohydrate given. The rate-limiting step, therefore, is the rate of uptake through the intestinal wall, rather than the hydrolysis of the carbohydrate.
The effects of dietary intake of sucrose versus the use of sodium cyclamate were studied in 10 Type 1 (insulin-dependent) diabetic patients on continuous subcutaneous insulin infusion therapy. After a 4-week run-in period, the patients were randomly assigned to a cross-over protocol with two 4-week periods during which they used sucrose or sodium-cyclamate as sweetener. During the experimental periods, 24 +/- 13 g/day sucrose and 348 +/- 270 mg/day of sodium cyclamate were consumed, respectively. Metabolic control was monitored by the patients performing blood glucose self-monitoring several times daily. Bi-weekly, all patients were followed-up in our outpatient clinic. Mean daily blood glucose concentrations as well as the average daily insulin dose did not differ between the three experimental periods. HbA1c-levels, serum lipids and body weight remained unchanged and within the normal ranges throughout the study. Thus, moderate dietary intake of sucrose did not affect metabolic control in these normal weight, near-normoglycaemic, normolipidaemic, pump-treated Type 1 diabetic patients during a 1-month period. Whether similar conclusions apply to less well controlled diabetic patients remains to be seen.
Earlier work shows that hyperlipemic type II diabetics tolerate wide ranges of sucrose and carbohydrate intake without effects on glycemic control, but a rise of fasting serum triglycerides sometimes occurs. To address further the issue of individual susceptibility to carbohydrate, the current study was designed to use each patient as his own control when given diets widely varying in sucrose content. After a stabilization period in the hospital on a normal sucrose content diet, each subject was given either a very low sucrose (less than 3 gm/day)-low carbohydrate (38 +/- 2%) diet or a high sucrose (220 gm)-high carbohydrate (63 +/- 3%) diet for 4 weeks. On a separate admission the opposite diet was assessed, again after an initial normal sucrose content diet. No consistent differences occurred in serum glucose levels or in 24-hr urinary glycosuria. High sucrose-carbohydrate intake raised fasting hypertriglyceridemia after 2 weeks but less thereafter. Severe sucrose-carbohydrate restriction did not significantly decrease fasting serum triglycerides; postprandial triglycerides changed in a trend opposite to fasting levels. No differences occurred in fasting serum insulin or serum cholesterol levels, but postprandial insulin levels were higher in high sucrose-carbohydrate diets. A diet with low sucrose and low total carbohydrate appears to offer no improvement in glycemic control over at least 70-fold higher dietary sucrose levels. However, high sucrose and carbohydrate diets increase fasting triglyceride levels in hypertriglyceridemic type II diabetics.
A critical review composed of two parts: estimates of present levels of sugars intake and of recent trends in nutritive carbohydrate sweetener content of the food supply and a review of recent scientific literature addressing potentially adverse health effects associated with sugars consumption. The review contains an executive summary, an appendix with 75 tables summarizing the estimation of sugars intake of U.S. population groups, and over one thousand citations.
The effects of variations in dietary carbohydrate and fat intake on various aspects of carbohydrate and lipid metabolism were studied in patients with non-insulin-dependent diabetes mellitus (NIDDM). Two test diets were utilized, and they were consumed in random order over two 15-day periods. One diet was low in fat and high in carbohydrate, and corresponded closely to recent recommendations made by the American Diabetes Association (ADA), containing (as percent of total calories) 20 percent protein, 20 percent fat, and 60 percent carbohydrate, with 10 percent of total calories as sucrose. The other diet contained 20 percent protein, 40 percent fat, and 40 percent carbohydrate, with sucrose accounting for 3 percent of total calories. Although plasma fasting glucose and insulin concentrations were similar with both diets, incremental glucose and insulin responses from 8 a.m. to 4 p.m. were higher (p less than 0.01), and mean (+/- SEM) 24-hour urine glucose excretion was significantly greater (55 +/- 16 versus 26 +/- 4 g/24 hours p less than 0.02) in response to the low-fat, high-carbohydrate diet. In addition, fasting and postprandial triglyceride levels were increased (p less than 0.001 and p less than 0.05, respectively) and high-density lipoprotein (HDL) cholesterol concentrations were reduced (p less than 0.02) when patients with NIDDM ate the low-fat, high-carbohydrate diet. Finally, since low-density lipoprotein (LDL) concentrations did not change with diet, the HDL/LDL cholesterol ratio fell in response to the low-fat, high-carbohydrate diet. These results document that low-fat, high-carbohydrate diets, containing moderate amounts of sucrose, similar in composition to the recommendations of the ADA, have deleterious metabolic effects when consumed by patients with NIDDM for 15 days. Until it can be shown that these untoward effects are evanescent, and that long-term ingestion of similar diets will result in beneficial metabolic changes, it seems prudent to avoid the use of low-fat, high-carbohydrate diets containing moderate amounts of sucrose in patients with NIDDM.
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.
This study addresses the metabolic effects of sucrose in the diets of 11 individuals with noninsulin-dependent diabetes mellitus (NIDDM). Each of two dietary periods were 15 days in length, and contained 50% of the calories as carbohydrate, 30% as fat, and 20% as protein. The only variable between the two periods was the percentage of total calories as sucrose, 16% v 1%. Fasting blood samples were analyzed for plasma glucose and insulin as well as total plasma VLDL-, LDL- and HDL-cholesterol and triglyceride concentrations. In addition, postprandial blood samples were obtained for the measurement of plasma glucose, insulin and triglyceride concentrations. Fasting plasma glucose, insulin, and day-long insulin concentrations were similar between the two diets. However, the addition of sucrose in amounts comparable to those typically consumed by the general population resulted in significantly elevated day-long glucose (P less than 0.05) and triglyceride (P less than 0.05) responses, as well as elevated fasting total plasma cholesterol (P less than 0.001), triglyceride (P less than 0.05), VLDL-cholesterol (P less than 0.01), and VLDL-triglyceride (P less than 0.05) concentrations. LDL-cholesterol and HDL-cholesterol concentrations were unchanged during the added sucrose diet. It is clear that the consumption of diets containing moderate amounts of sucrose resulted in changes to plasma lipid and postprandial glucose concentrations that have been identified as risk factors for coronary artery disease. Therefore, it seems prudent at this time to advise patients with NIDDM to avoid added dietary sucrose.
Eighteen healthy young men on an Antarctic base were observed for 10 months. For a baseline period of 4 weeks they received a normal diet, then they were put on an isocaloric, virtually sucrose-free diet for a period of 14 weeks, and this was followed by a further period of 24 weeks on the normal diet. They took all their meals together, and the diet was found generally acceptable. Estimations were made, on fasting serum samples, of triglyceride, total cholesterol, and phospholipid levels. In those men with higher triglyceride levels on the normal diet (>120 mg. per 100 ml.) there was a significant fall in triglyceride levels during the sucrose-free period, whilst there was no significant change in triglyceride levels in the men with lower triglyceride levels (<120 mg. per 100 ml.). Smaller changes occurred in total cholesterol and phospholipid levels. Such weight changes as occurred were not significant and did not correlate with changes in lipid levels.
1. Fasting serum cholesterol and triglyceride, and post prandial insulin secretion and lipaemia were measured in human subjects in a metabolic ward, who were given an ordinary diet (diet 1) in which the sucrose was isocalorically replaced by starch (diet 2) or vice versa. The subjects were nine healthy normolipaemic adult males. In eight of these subjects the effect of sucrose calorie reduction (diet 3) on fasting serum lipids was also studied. 2. When starch replaced sucrose, there were no singnificant differences in fasting serum lipid concentrations or immunoreactive insulin or in the insulin response and alimentary lipaemia after a standard mixed breakfast. 3. Serum triglyceride concentration fell and cholesterol concentration rose during the period of sucrose (and calorie) restriction. 4. After lunch and supper on the first two diets (when different carbohydrates were given) the lipaemic response was larger and the insulin response smaller after meals containing sucrose. 5. Thus, there was no difference between concentrations of fasting serum lipids when starch replaced sucrose at 23% total calories, but the concentrations of serum triglycerides were higher after individual mixed meals containing sucrose. 6. There were no significant differences in the fatty acid patterns of serum lipids on the different diets.
A group of 101 diabetic patients containing equal numbers of patients with and without clinical atherosclerosis and 104 control subjects of similar age and sex were studied. The diabetic patients with atherosclerosis were found to have higher triglyceride and cholesterol levels, higher insulin-glucose ratios, and a higher frequency of pre-β band staining on lipoprotein electrophoresis than diabetic patients without atherosclerosis or control subjects. Diabetic patients with atherosclerosis could be discriminated better from those without atherosclerosis by the use of triglyceride levels than by the use of cholesterol levels. Segregated arbitrarily into three categories of body weight, diabetic patients with atherosclerosis had higher triglyceride levels than similarly classified diabetic patients without atherosclerosis. Basal insulin levels, triglyceride levels, and indices of body weight were highly intercorrelated in the diabetic patients with atherosclerosis. However, fasting levels of serum insulin were similar in the two groups of diabetic patients. There was no clear relationship
1. The effects of isocalorically exchanging dietary starch and sucrose on glucose tolerance, plasma insulin and serum lipids were examined in nine middle-aged subjects. A ‘sucrose’ period in which 70% of dietary carbohydrate was supplied as sucrose was alternated with a ‘sucrose free’ period in which dietary carbohydrate was supplied mainly as starch. Each period lasted 4 weeks; eleven balances were completed. 2. Changes in body weight during the balances were small and statistically insignificant. 3. Fasting blood sugar levels were significantly elevated during the ‘sucrose’ period. During 50 g glucose tolerance tests, blood sugar levels were slightly higher during the ‘sucrose’ period but this difference was not statistically significant. 4. Plasma insulin levels were similar during the dietary periods, both in the fasting state and after 50 g of glucose. 5. Mean levels of serum cholesterol, serum triglyceride and plasma NEFA showed no significant differences between the two dietary periods. 6. It is concluded that glucose tolerance, plasma insulin and serum lipids are not significantly altered by the substitution of sucrose for starch at levels of sucrose intake comparable to those in the Western diet.
In the Whitehall Study of 18,403 male civil servants aged 40--64 years, 7 1/2 year coronary-heart-disease (CHD) mortality has been examined in relation to blood-sugar concentration 2 h after a 50 g oral glucose load. CHD mortality was approximately doubled for subjects with inpaired glucose tolerance (IGT), defined as a blood-sugar above the 95th centile (greater than or equal to 96 mg/dl). There was no trend of CHD mortality with blood-sugar below the 95th centile. Within the IGT group, age, systolic blood-pressure, and ECG abnormality (Whitehall criteria) were significantly predictive of subsequent CHD mortality. These findings are relevant to discussions on the criteria for diabetes which include the definition of an IGT category with increased risk of large-vessel disease, but without the high risk of small-vessel disease as occurs in diabetes mellitus.
The hyperglycaemic effect of 20 g sucrose taken at the end of a regular mixed meal by diabetic patients was measured in six adult type 1 diabetics, C-peptide negative, controlled by the artificial pancreas, and twelve adult type 2 diabetics, with fasting plasma glucose levels below 7.2 mmol/l (130 mg/100 ml) and post-prandial plasma glucose levels below 10.0 mmol/l (180 mg/100 ml), treated by diet alone or with glibenclamide and/or metformin. All the patients were given on consecutive days, in random order, two mixed meals of grilled meat, green beans, and cheese, as well as a cake made either of rice, skimmed milk, and saccharine (meal A) or rice, skimmed milk, and 20 g sucrose (meal B). The meals contained equal amounts of calories and of carbohydrate. There was no difference between the meals in plasma glucose curves and plasma insulin or insulin infusion rate variations whether in peak values, peaking times, or areas under the curves, in either group of patients. Sparing use of sucrose taken during mixed meals might help well-controlled diabetic patients to comply with their daily dietary prescription while maintaining good blood glucose control.
The determine the effect of different foods on the blood glucose, 62 commonly eaten foods and sugars were fed individually to groups of 5 to 10 healthy fasting volunteers. Blood glucose levels were measured over 2 h, and expressed as a percentage of the area under the glucose response curve when the same amount of carbohydrate was taken as glucose. The largest rises were seen with vegetables (70 +/- 5%), followed by breakfast cereals (65 +/- 5%), cereals and biscuits (60 +/- 3%), fruit (50 +/- 5%), dairy products (35 +/- 1%), and dried legumes (31 +/- 3%). A significant negative relationship was seen between fat (p less than 0.01) and protein (p less than 0.001) and postprandial glucose rise but not with fiber or sugar content.
To examine whether the form of dietary carbohydrate influences glucose and insulin responses, we studied the glucose and insulin responses to five meals--each containing a different form of carbohydrate but all with nearly identical amounts of total carbohydrate, protein, and fat--in 10 healthy subjects, 12 patients with Type I diabetes, and 10 patients with Type II diabetes. The test carbohydrates were glucose, fructose, sucrose, potato starch, and wheat starch. In all three groups, the meal containing sucrose as the test carbohydrate did not produce significantly greater peak increments in the plasma concentration of glucose or greater increments in the area under the plasma glucose-response curves than did meals containing potato, wheat, or glucose as test carbohydrates. Urinary excretion of glucose in patients with diabetes was not significantly greater after the sucrose meal. The meal containing fructose as the test carbohydrate produced the smallest increments in plasma glucose levels, but the differences were not always statistically significant. In healthy subjects and patients with Type II diabetes, peak serum concentrations of insulin were not significantly different in response to the five test carbohydrates. Our data do not support the view that dietary sucrose, when consumed as part of a meal, aggravates postprandial hyperglycemia.
We investigated the effect of ice cream ingestion on blood glucose control in conventionally treated and intensively treated insulin-dependent (type I) diabetic patients. After the ingestion of 100 g of ice cream, plasma glucose excursions as measured by the peak increment (90 +/- 30 mg/dL) and area under the curve (166 +/- 59 mg/dL X hour) were modest and not significantly different between the subgroups of intensively treated and conventionally treated diabetics. A small dose (3 to 5 units) of rapid-acting insulin given 30 minutes before ingestion of ice cream reduced the modest plasma glucose excursion. A modest amount of ice cream may be included in weight-maintaining diets of insulin-dependent diabetics. Small doses of rapid-acting insulin prevent any adverse effect of the ice cream on blood glucose control.
To further understand the effect of high carbohydrate (CHO)-low fat diets and the role of variations in dietary sucrose on CHO and lipid metabolism, 10 patients with hypertriglyceridemia were fed 2 isocaloric, typical American diets, containing 40% and 60% CHO, for 15 days in random sequence. Each patient was their own control, and they were divided into 2 groups of 5 patients each. In one group, sucrose was held constant at 13% of total calories (40-13% and 60-13%), whereas the sucrose content was 9% of the total calories on a 40% CHO diet (40-9%), and 15% of total calories on a 60% CHO diet (60-15%) in the other group. Fasting and postprandial blood samples were analyzed for plasma glucose, insulin, cholesterol (Chol), and triglycerides (TG), as well as for Chol and TG in chylomicrons, very low density, low density, and high density lipoproteins (HDL). Fasting plasma TG levels were significantly increased in both groups on the 60% CHO diet, primarily due to increases in very low density-TG concentration. The magnitude of the elevation was attenuated when sucrose content was kept constant. Postprandial TG responses were qualitatively similar. There were no significant changes in plasma Chol concentrations, except for a modest fall in plasma HDL-Chol level after the 60-13% diet period (P less than 0.05). No significant differences were found in fasting plasma glucose or insulin concentration. However, postprandial glucose and insulin responses were increased on both high CHO diets. The results of these studies demonstrate that high CHO-low fat diets, in general, tend to elevate plasma glucose, insulin, and TG concentrations and reduce HDL-Chol concentration in patients with endogenous hypertriglyceridemia. In addition, these data illustrate the important role that small variations in dietary sucrose can play in modulation of CHO and lipid metabolism.
Overtly hypertriglyceridemic patients with non-insulin-dependent diabetes mellitus were given a control diet containing 120 g of sucrose and 50 percent carbohydrate, and later randomly assigned to receive isocaloric high- (220 g), intermediate- (120 g), or low- (less than 3 g) sucrose/carbohydrate diets for four weeks. The low-sucrose diet group demonstrated a modest but significant decrease in mean fasting serum glucose level in the first week only, although this change was no different from the other two dietary groups and was not sustained. All groups had little change in late postprandial serum glucose levels from control values, and no significant alterations in 24-hour glycosuria. The high-sucrose diet group demonstrated a significant increase in fasting serum triglyceride levels by the second week of the study, whereas the intermediate- and low-sucrose diet groups showed a decrease in mean fasting triglyceride levels. In contrast, the low-sucrose diet group's late postprandial serum triglyceride levels increased by the fourth week, whereas levels fell in the high-sucrose diet group. Mean fasting serum cholesterol concentrations decreased from control values in the high-sucrose diet group. Thus, although very high sucrose and carbohydrate consumption is clearly deleterious to fasting tryglyceride levels in non-insulin-dependent diabetes mellitus with preexisting hypertriglyceridemia, it appears that low dietary sucrose and carbohydrate proportions do not further improve preprandial glycemia and glycosuria and may adversely affect late postprandial serum triglyceride concentration. This study suggests that isocaloric sucrose and carbohydrate restriction below usual daily levels (120 g per day) offers no consistent benefit in glycemia or lipid control in overt type II diabetes.
In 9 of the 14 national samples of diabetic patients assembled for the WHO Multinational Study of Vascular Disease in Diabetes additional laboratory data made it possible to relate manifestations of macrovascular disease to blood glucose concentrations as well as to diabetes duration and to other potential determinants. In five of the samples, serum triglyceride concentrations were also measured and were included in simple and multivariate analyses. Ischemic heart disease defined from Minnesota-coded EKGs and standardized WHO questionnaires was more strongly associated with serum triglyceride concentrations than with serum cholesterol concentrations, an association less notable in non-insulin-dependent diabetic patients. Ischemic heart disease was not related to the single fasting plasma glucose estimated for this study. Stroke and amputation were much more strongly related to the known duration of diabetes than was ischemic heart disease, and they were both related to blood glucose concentration measured at the time of study. Despite major variation in arterial disease prevalence rates between collaborating centers, risk for diabetic women appeared to equal that for diabetic men. The major variation in arterial disease prevalence between national groups could be accounted for only in part by the risk factors studied. Other factors, genetic or more likely environmental, are likely to contribute to the variation in arterial disease susceptibility and, if definable, may be potentially preventable.
The effects of dietary sucrose on blood lipids and their distribution in lipoprotein fractions were determined in 12 males and 12 females diagnosed as carbohydrate-sensitive on the basis of an exaggerated insulin response to a sucrose load. The subjects were fed diets containing 5%, 18% or 33% of the total calories as sucrose for 6 weeks each in a crossover design. Initial body weights were essentially maintained. Total fasting triglycerides of males, but not females, increased significantly as the level of sucrose in the diet increased. Triglycerides in males averaged 132% more than in females and were significantly greater at all three levels of sucrose. Significant increases in total cholesterol, VLDL cholesterol, LDL cholesterol, and HDL cholesterol were observed as the sucrose content of the diet increased. HDL cholesterol ratios decreased significantly in males as sucrose increased and for 5%, 18% and 33% were 0.34, 0.32 and 0.27, respectively. Abnormal lipoprotein phenotypes were most common when the subjects consumed 33% sucrose and least common when they consumed 5% sucrose. These results indicate that sucrose intake at levels now common in the American diet by carbohydrate-sensitive males could lead to a blood lipid profile associated with coronary risk.
We studied the acute effects of oral ingestion of 50-g loads of dextrose, sucrose, and fructose on post-prandial serum glucose, insulin, and plasma glucagon responses in 9 normal subjects, 10 subjects with impaired glucose tolerance, and 17 non-insulin-dependent diabetic subjects. The response to each carbohydrate was quantified when the respective carbohydrate was given alone in a drink or when given in combination with protein and fat in a test meal. The data demonstrate that (1) fructose ingestion resulted in significantly lower serum glucose and insulin responses than did sucrose or dextrose ingestion in all study groups, either when given alone or in the test meal; (2) although fructose ingestion always led to the least glycemic response compared with the other hexoses, the serum glucose response to fructose was increased the more glucose intolerant the subject; (3) urinary glucose excretion during the 3 h after carbohydrate ingestion was greatest after dextrose and least after fructose in all groups. In conclusion, fructose ingestion results in markedly lower serum glucose and insulin responses and less glycosuria than either dextrose or sucrose, both when given alone or as a constituent in a test meal. However, as glucose tolerance worsens, an increasingly greater glycemic response to fructose is seen.
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.
Influences of dietary fructose and sucrose on serum triglycerides in hypertriglyceridemia and diabe-tetes
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Crapo PA, Kolterman OG, OlefskyJM: Effects of oral fruc-tose in normal, diabetic, and impaired glucose tolerance subjects. Diabetes Care 3:575-81, 1980
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Risk factors for my-ocardial infarction in the Stockholm perspective studies: a 14-year follow-up focusing on the role of plasma tri-glyceride and cholesterol
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Carlson LA, Bottiger LE, Ahfeldt PE: Risk factors for my-ocardial infarction in the Stockholm perspective studies: a 14-year follow-up focusing on the role of plasma tri-glyceride and cholesterol. Ada Med Scand 206:351-60, 1979
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American Diabetes Association: Clycemic effects of carbohydrates
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