Abstract
Type 2 diabetes has become the most frequently encountered metabolic disorder in the world and obesity, meaning visceral adiposity, is the core problem. In the abdominal adipose tissue, insulin resistance (IR) reduces the antilipolytic effect of insulin, which in turn leads to reduced glucose uptake and increased release of free fatty acids (FFAs) and glycerol. Chronic exposure of beta cells to elevated FFA levels causes detrimental consequences such as increased insulin secretion at low glucose concentrations, decreased proinsulin biosynthesis, depletion of insulin reserves and reduced response to concentrations of glucose stimulus. Adipose peroxisome proliferator-activated receptors (PPAR)-γ appears to be an essential mediator for the maintenance of whole-body insulin sensitivity that protects non-adipose tissue against lipid overload. Current data suggest that PPAR-γ-activating ligands improve adipose tissue function, and may prevent the progression of IR to diabetes and also endothelial dysfunction to atherosclerosis. Links between environmental influences, the layout of visceral fat, the PPARs, the adiponectin and the adipocytokines still need to be completely clarified.
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