Liese AD, Schulz M, Fang F, Wolever TMS, D’Agostino Jr RB, Sparks KC. Dietary glycemic index and glycemic load, carbohydrate and fiber intake, and measures of insulin sensitivity, secretion, and adiposity in the Insulin Resistance Atherosclerosis Study. Diabetes Care 28, 2832-2838

Universität Potsdam, Potsdam, Brandenburg, Germany
Diabetes Care (Impact Factor: 8.42). 01/2006; 28(12):2832-8. DOI: 10.2337/diacare.28.12.2832
Source: PubMed


We studied the association of digestible carbohydrates, fiber intake, glycemic index, and glycemic load with insulin sensitivity (S(I)), fasting insulin, acute insulin response (AIR), disposition index, BMI, and waist circumference.
Data on 979 adults with normal (67%) and impaired (33%) glucose tolerance from the Insulin Resistance Atherosclerosis Study (1992-1994) were analyzed. Usual dietary intake was assessed via a 114-item interviewer-administered food frequency questionnaire from which nutrient intakes were estimated. Published glycemic index values were assigned to food items and average dietary glycemic index and glycemic load calculated per subject. S(I) and AIR were determined by frequently sampled intravenous glucose tolerance test. Disposition index was calculated by multiplying S(I) with AIR. Multiple linear regression modeling was employed.
No association was observed between glycemic index and S(I), fasting insulin, AIR, disposition index, BMI, or waist circumference after adjustment for demographic characteristics or family history of diabetes, energy expenditure, and smoking. Associations observed for digestible carbohydrates and glycemic load, respectively, with S(I), insulin secretion, and adiposity (adjusted for demographics and main confounders) were entirely explained by energy intake. In contrast, fiber was associated positively with S(I) and disposition index and inversely with fasting insulin, BMI, and waist circumference but not with AIR.
Carbohydrates as reflected in glycemic index and glycemic load may not be related to measures of insulin sensitivity, insulin secretion, and adiposity. Fiber intake may not only have beneficial effects on insulin sensitivity and adiposity, but also on pancreatic functionality.

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    • "Similarly, the role of dietary carbohydrates (carbs) has not been fully established or defined. Some studies have shown that carb-rich diets promote development of insulin resistance and T2DM [17],[18] while others have shown that high-carb diet is protective against insulin resistance and T2DM compared to HFD [19], and low-carb diet is not necessarily protective against insulin resistance and diabetes [20],[21]. These conflicting results demonstrate the complexity and difficulty in defining the role of each dietary component in insulin resistance and T2DM. "
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    ABSTRACT: Both dietary fat and carbohydrates (Carbs) may play important roles in the development of insulin resistance. The main goal of this study was to further define the roles for fat and dietary carbs in insulin resistance. C57BL/6 mice were fed normal chow diet (CD) or HFD containing 0.1-25.5% carbs for 5 weeks, followed by evaluations of calorie consumption, body weight and fat gains, insulin sensitivity, intratissue insulin signaling, ectopic fat, and oxidative stress in liver and skeletal muscle. The role of hepatic gluconeogenesis in the HFD-induced insulin resistance was determined in mice. The role of fat in insulin resistance was also examined in cultured cells. HFD with little carbs (0.1%) induced severe insulin resistance. Addition of 5% carbs to HFD dramatically elevated insulin resistance and 10% carbs in HFD was sufficient to induce a maximal level of insulin resistance. HFD with little carbs induced ectopic fat accumulation and oxidative stress in liver and skeletal muscle and addition of carbs to HFD dramatically enhanced ectopic fat and oxidative stress. HFD increased hepatic expression of key gluconeogenic genes and the increase was most dramatic by HFD with little carbs, and inhibition of hepatic gluconeogenesis prevented the HFD-induced insulin resistance. In cultured cells, development of insulin resistance induced by a pathological level of insulin was prevented in the absence of fat. Together, fat is essential for development of insulin resistance and dietary carb is not necessary for HFD-induced insulin resistance due to the presence of hepatic gluconeogenesis but a very small amount of it can promote HFD-induced insulin resistance to a maximal level.
    Full-text · Article · Jul 2014 · PLoS ONE
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    • "For calculating glycemic load, the amount of GI is multiplied by carbohydrate amount in gram.[13] Several studies have been conducted on the relationship of these two indices with obesity in adults and have reported a direct, neutral or reverse relationship, and their results were controversial.[141516171819] DASH diet is one of the investigated topics that appear to have a low level of GI due to having high fruit, vegetable and whole grain ingredients.[20] "
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    ABSTRACT: Several evidences have been reported so far in terms of the relationship between obesity and glycemic index and glycemic load in children. However, the number of review studies that have dealt with recent findings is quite low. The purpose of present study is to review the existing evidences in this regard. FIRST OF ALL, THE PHRASES: "Glycaemic index", "Glycaemic load", "Glycemic index" OR "Glycemic load" accompanied by one of the words: "Adolescent", "Young", "Youth" "Children" OR "Child" were searched in texts of articles existing in ISI and PUBMED databases which were obtained out of 1001 articles. Among these, some articles, which reviewed the relationship of obesity with glycemic index and glycemic load, were selected. Finally, 20 articles were studied in current review study. The majority of cross-sectional studies have found children's obesity directly linked with glycemic index and glycemic load; however, cohort studies found controversial results. Also, the intervention studies indicate the negative effect of glycemic index and glycemic load on obesity in children. Published evidences reported inconsistent results. It seems that existing studies are not sufficient and more studies are needed in this regard.
    Full-text · Article · Jan 2014
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    • "Another limitation is related to glycemic control. Although some studies showed that the amount of carbohydrate is the main concern rather than GI or GL in diabetic patient's diet [54, 55], others yet advice to prescribe a low-GI and GL diet for diabetics [47–49]. The entry of tryptophan into the brain is also related to its plasma concentration to the sum of the other large neutral amino acids (Trp/LNAAs ratio) (LNAAs: tyrosine, phenylalanine, leucine, isoleucine, valine, and methionine) [56]. "
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    ABSTRACT: There is a bidirectional adverse association between diabetes and depression. The odds for experiencing depressive symptoms in diabetic patients are two times more than nondiabetic persons, and depression is an independent predictor for the onset of diabetes. However, depression has been approximately unrecognized and untreated in two-thirds of diabetic patients, which may lead to worsened diabetes complications. A cornerstone strategy for managing depression among diabetic patients is the use of diet to improve both health problems. Because of similar pathophysiology for chronic diseases and depression, it seems that similar dietary recommendations could be useful. However, few studies have been conducted among diabetic patients. Regarding the complications of diabetes such as renal diseases and coronary heart diseases, the proper range of various macronutrients should be clarified in depressed diabetic patients as well as the proper type of each macronutrient. In this paper, we reviewed the available data on the treatment of depression in diabetic patients.
    Full-text · Article · Sep 2013 · Journal of Diabetes Research
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