It is observed an inverse relationship between adiponectin and insulinsensivity. Adiponectin is similar in structure to TNF-α (tumor necrosis factor α) which paradoxically appears to be increased in abdominal adipose tissue. Increases in proinflammatory cytokines (interleukine 6, TNF-α, resistin, C- reactiv protein – CRP) reflect overproduction by the expanded adipose tissue mass [44,45]. All of these factors contribute to the exaggerated release of free fatty acids from abdominal adipocytes into the portal system. Free fatty acids have deleterious effects on insulin uptake by the liver and contribute to the increased hepatic gluconeogenesis and hepatic glucose release observed in central obesity [46].

High glucose levels have a glucotoxic effect on β-cells, probably as a result of free radical oxidative damage [47]. Hyperinsulinaemia may reduce β-cell function by causing excess amyloid deposits [48]. High free fatty acids levels lead to triacylglycerol accumulation in β-cells, which reduces insulin secretion [49]. Accordingly, by reducing hyperglycaemia, hyperinsulinemia and free fatty acids levels, low-GI foods may decrease the factors contributing to β-cell failure [23].

C. Dyslipidaemia

Hyperinsulinaemia and insulin resistance are significantly correlated to dyslipidaemia and contribute to the characteristic alteration of plasma lipid profile associated with obesity.

Low-GI diets may reduce insulin-stimulated activity of 5-hydroxi-3-methylglutaryl-CoA reductase, the rate-limiting enzyme involved in cholesterol synthesis, by reducing insulin levels. Dietary fiber tends to reduce bile acid and cholesterol re-absorption from the ileum, which may inhibit hepatic cholesterol synthesis [47].

Low-carbohydrates diets as well as low-fat diets significantly decreased several biomarkers of inflammation (CRP, TNF-α, IL-6), which play a key role in all stages of the pathogenesis of atherosclerosis [15].

D. Cardiovascular risk factors

Hyperglicaemia is a continuous risk factor for CVD morbidity and mortality.

The effects of cytokines on peripheral tissues with increased intracellular lipids also lower cellular insulin sensitivity: the surge in lipids promotes proliferation of the vasa vasorum of the arterial media and apoptosis by the medial macrophages with a further release of cytokines. There is an additional complex relationship through an associated pro-inflammatory state and alterations in coagulation. A rise in blood viscosity is induced by the release of profibrinogen and plasminogen activator inhibitor 1 from adipocytes with a fall in plasminogen activator. These changes may explain the role of obesity as a promoter of intracellular inflammatory processes that result in arterial damage. Ethnic differences in CRP may explain some of the variation observed in insulin resistance across populations with comparable weight gain and associated medical complications [46].

References