Dietary Glycemic Index and Glycemic Load Are Associated with Metabolic Control in Type 2 Diabetes: The CAPRI Experience

Department of Geriatrics and Metabolic Diseases, Second University of Naples, Naples, Italy.
Metabolic syndrome and related disorders (Impact Factor: 1.98). 02/2010; 8(3):255-61. DOI: 10.1089/met.2009.0096
Source: PubMed


The role of low-glycemic-index diets in the treatment of diabetes mellitus remains unclear. The aim of the present study was to evaluate the association between the dietary glycemic index (GI) and glycemic load (GL) with metabolic control in type 2 diabetic patients.
We conducted a cross-sectional analysis in 901 outpatients with type 2 diabetes attending diabetes clinics located in the area of the Campania County, South Italy, who provided complete home blood glucose profiles and centralized glycosylated hemoglobin A1c (HbA1c). Dietary information was obtained using semiquantitative food-frequency questionnaires. HbA1c was assessed in the centralized laboratory while blood glucose profiles were assessed at home.
After adjustment for age, body mass index (BMI), waist circumference, waist-to-hip ratio, smoking, alcohol consumption, physical activity, medication use, prevalence of metabolic syndrome, hypertension, energy and fiber intake, dietary GI and GL were positively associated with HbA1c in a dose-dependent fashion (P for trend, 0.007 for GI and 0.02 for GL). Diabetic patients with the highest GI and GL had the highest HbA1c levels (difference 1%, P = 0.001). The difference in 1-h postmeal glucose levels at home between the highest and the lowest quintile of GI was 37 (15) [mean and standard deviation (SD)] mg/dL (P = 0.001).
Diets low in GI and GL are associated with lower HbA1c and postmeal glucose levels in the everyday life of type 2 diabetic patients.

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    • "Fasting and postprandial blood glucose remained below 100 mg/dL among all participants throughout the entire study, which is similar to findings reported in previous studies (Bellisle et al., 2007; Esposito et al., 2010; Perälä et al., 2011). This may be due to the predominance of low-GI foods (fiber-rich whole grains), despite the ingestion of foods with a medium to high GI. "
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    ABSTRACT: References: this document contains references to 75 other documents. To copy this document: The fulltext of this document has been downloaded 2 times since 2014* Access to this document was granted through an Emerald subscription provided by 478417 [] For Authors If you would like to write for this, or any other Emerald publication, then please use our Emerald for Authors service information about how to choose which publication to write for and submission guidelines are available for all. Please visit for more information. About Emerald Emerald is a global publisher linking research and practice to the benefit of society. The company manages a portfolio of more than 290 journals and over 2,350 books and book series volumes, as well as providing an extensive range of online products and additional customer resources and services. Emerald is both COUNTER 4 and TRANSFER compliant. The organization is a partner of the Committee on Publication Ethics (COPE) and also works with Portico and the LOCKSS initiative for digital archive preservation. Abstract Purpose – The purpose of the paper is to determine the effects of a hypocaloric diet with a low-glycaemic index (GI) on weight loss and postprandial blood glucose and assess both the satiety and palatability of the diet. Design/methodology/approach – A clinical trial was conducted with ten women (mean age: 38.8711.3 years; body mass index: 27.273.5 kg/m
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    • "Author's personal copy type 2 diabetes (Esposito et al., 2010). It is possible that an increase in GLP-1 contributes to these metabolic improvements, as low-GI carbohydrates exhibit a lower absorption rate and, therefore, have the potential to give rise to interaction of nutrients with more distal regions of the small intestine. "
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    ABSTRACT: The delivery of nutrients from the stomach into the duodenum and their subsequent interaction with the small intestine to stimulate incretin hormone release are central determinants of the glycemic response. The incretin effect has hitherto been attributed to the secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells in the intestinal epithelium. A number of recent studies have yielded fundamental insights into the influence of individual nutrients on incretin release and the mechanisms involved in the detection of carbohydrates, fats, and proteins by enteroendocrine cells, including the K(ATP) channel, sodium-glucose cotransporter 1 (SGLT1), sweet taste receptors, G-protein-coupled receptors (GPRs), and oligopeptide transporter 1 (PepT1). Dietary modification, including modifying macronutrient composition or the consumption of "preloads" in advance of a meal, represents a novel approach to manipulate the incretin response and thereby regulate glucose homeostasis in patients with type 2 diabetes. This review focuses on the effects of individual nutrients on incretin hormone secretion, our current understanding of the signaling mechanisms that trigger secretion by enteroendocrine cells, and the therapeutic implications of these observations.
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