Abstract
Identifying the causative relationship between the fatty acid composition of cell membranes and type 2 diabetes mellitus fundamentally contributes to the understanding of the basic pathophysiological mechanisms of the disease. Important outcomes of the reviewed studies appear to support the hypotheses that the flexibility of a membrane determined by the ratio of (poly)unsaturated to saturated fatty acyl chains of its phospholipids influences the effectiveness of glucose transport by insulin-independent glucose transporters (GLUTs) and the insulin-dependent GLUT4, and from the prediabetic stage on a shift from unsaturated towards saturated fatty acyl chains of membrane phospholipids directly induces a decrease in glucose effectiveness and insulin sensitivity. In addition, it has become evident that a concomitant increase in stiffness of both plasma and erythrocyte membranes may decrease the microcirculatory flow, leading ultimately to tissue hypoxia, insufficient tissue nutrition, and diabetes-specific microvascular pathology. As to the etiology of type 2 diabetes mellitus, a revised hypothesis that attempts to accommodate the reviewed findings is presented.
Highlights
This report continues our analyses of the biochemical factors playing an important role in the pathogenesis of gestational diabetes mellitus (GDM) and type 2 diabetes mellitus, that is, a relationship among insulin sensitivity, glucose effectiveness, and membrane flexibility [1]
Assessment of these parameters has revealed that type 2 diabetes mellitus and its prediabetic phase are characterised by a decrease in both glucose effectiveness and insulin sensitivity [2]
The goal of this paper is to provide a basis for understanding the intimate association of type 2 diabetes mellitus characterised by insulin sensitivity and glucose effectiveness, and the mechanical effects of a shift from unsaturated towards saturated fatty acids in membrane phospholipids on these entities
Summary
This report continues our analyses of the biochemical factors playing an important role in the pathogenesis of gestational diabetes mellitus (GDM) and type 2 diabetes mellitus, that is, a relationship among insulin sensitivity, glucose effectiveness, and membrane flexibility [1]. The minimal model of glucose disappearance from a frequently sampled intravenous glucose tolerance test will be the key to assessing insulin sensitivity and glucose effectiveness in vivo, in physiological, pathophysiological, and epidemiological studies [2]. Assessment of these parameters has revealed that type 2 diabetes mellitus and its prediabetic phase are characterised by a decrease in both glucose effectiveness and insulin sensitivity [2]. The goal of this paper is to provide a basis for understanding the intimate association of type 2 diabetes mellitus characterised by insulin sensitivity and glucose effectiveness, and the mechanical effects of a shift from unsaturated towards saturated fatty acids in membrane phospholipids on these entities
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