The role of endothelial dysfunction driven by adipocitokines in the development and progression of microvascular complications in patients with type 1 and type 2 diabetes.

Micro and macrovascular complications are the leading cause of morbidity and mortality in diabetic patients. During the last decades attention has been focused on their early diagnosis and prevention. Diabetes related metabolic abnormalities: insulin resistance, hyperglycaemia and dyslipidaemia along with oxidative stress and low-grade inflammation contribute to the development of endothelial dysfunction and macrovascular complications. Recent investigations indicate a potential role of adipocitokines originating from visceral adipose tissue: adiponectin, leptin, resistin and dipepetidyl peptidase-4 (DPP-4) activity in the development of microvascular complications in diabetes. The association of these adipocitokines with the activity of endothelial synthetase (eNOS) involved into the metabolism of nitric oxide (NO) was documented in animal and cell culture studies. We hypothesize that lower adiponectin and higher leptin and resistin plasma concentration and DPP-4 activity are associated with the development and progression of diabetic microvascular complications by endothelial function impairment. A possible identification of new markers of the complex pathophysiology development and progression of microvascular complications in diabetes will contribute to improved diagnosis followed by an individualized patients approach.