Reviews

Macronutrient Composition and Management of Non-Insulin-Dependent Diabetes Mellitus (NIDDM): A New Paradigm for Individualized Nutritional Therapy in Diabetes Patients

Efi Koloverou, Demosthenes B. Panagiotakos

Abstract

Medical nutrition therapy constitutes an important lifestyle intervention in diabetes management. Several nutrition patterns have been effective in improving diabetes control, but there has been a debate about the optimal macronutrient composition in diabetes meal planning. For many years, the recommended diets for persons with and without diabetes were similar, i.e. heart-healthy and low in fat. For almost three decades, carbohydrates have been lauded, lipids demonized, and proteins considered of little importance. However, in the past few years, this concept has been questioned and reassessed. Modern nutritional recommendations for people with diabetes are headed towards individualization, but lack specific guidelines. Nutritional algorithms may help nutritionists in diabetes meal planning. This review aims to discuss: 1) the effects of the three major macronutrients (carbohydrates, proteins, and lipids) on glucose levels, 2) current recommendations for macronutrient intake for people with diabetes, and 3) specific parameters that need to be taken into consideration when determining the macronutrient composition for a person with diabetes, for example body mass index, degree of insulin resistance, HbA1c value, and lipid profile (especially triglycerides and HDL cholesterol). These aspects are analyzed in the context of the results of recent studies, especially randomized controlled trials (RCTs). Finally, we introduce an individualized nutritional concept that proposes carbohydrate over lipid restriction, substitution of SFAs with MUFAs and PUFAs, and adequate intake of dietary fiber, which are key factors in optimizing diabetes management.

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Understanding Genetic Heterogeneity in Type 2 Diabetes by Delineating Physiological Phenotypes: SIRT1 and its Gene Network in Impaired Insulin Secretion

Shafat Ali¹, Shazia Nafis¹, Ponnusamy Kalaiarasan¹, Ekta Rai², Swarkar Sharma², Rameshwar N. Bamezai¹

Abstract

Type 2 diabetes (T2D) is a chronic metabolic disease which shows an exponential increase in all parts of the world. However, the disease is controllable by early detection and modified lifestyle. A series of factors have been associated with the pathogenesis of diabetes, and genes are considered to play a critical role. The individual risk of developing T2D is determined by an altered genetic background of the en-zymes involved in several metabolism-related biological mechanisms, including glucose homeostasis, insulin metab-olism, the glucose and ion transporters involved in glucose uptake, transcription factors, signaling intermediates of insulin signaling pathways, insulin production and secretion, pancreatic tissue development, and apoptosis. However, many candidate genes have shown heterogeneity of associations with the disease in different populations. A possible approach to resolving this complexity and under-standing genetic heterogeneity is to delineate the physiological phenotypes one by one as studying them in combination may cause discrepancies in association studies. A systems biology approach involving regulatory proteins, transcription factors, and microRNAs is one way to understand and identify key factors in complex diseases such as T2D. Our earlier studies have screened more than 100 single nucleotide polymorphisms (SNPs) belonging to more than 60 globally known T2D candidate genes in the Indian population. We observed that genes invariably involved in the activity of pancreatic β-cells provide susceptibility to type 2 diabetes (T2D). Encouraged by these results, we attempted to delineate in this review one of the commonest physiological phenotypes in T2D, namely impaired insulin secretion, as the cause of hyperglycemia. This review is also intended to explain the genetic basis of the pathophysiology of insulin secretion in the context of variations in the SIRT1 gene, a major switch that modulates insulin secretion, and a set of other genes such as HHEX, PGC-α, TCF7L2, UCP2, and ND3 which were found to be in association with T2D. The review aims to look at the genotypic and transcriptional regulatory relationships with the disease phenotype.

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