Plasma Adiponectin and Resistin Levels in Type 2 Diabetic Obese Female Patients With and Without Hypertension and Retinopathy

摘要

Background: In the past, adipose tissue was largely regarded as a depot for fuel storage in the form of triglyceride. However, adipose tissue is an active endocrine organ that secretes a variety of metabolically important substances including adipokines. The adipocyte is now known to secrete a variety of proteins such as tumour necrosis factor (TNF)- , adipsin, plasminogen activator inhibitor-1, leptin, resistin, and adiponectin. Adipose tissue regulates insulin sensitivity via the circulating adipocytokines, resistin and adiponectin. These factors affect insulin sensitivity and may represent a link between obesity, insulin resistance and type 2 diabetes (DM). The objective of this study was to compare the levels of resistin and adiponectin in type 2 diabetic obese female patients with and without hypertension and retinopathy. Subjects and Methods: In this study the plasma adiponectin and resistin concentrations were investigated, in 20 control obese non-diabetic females and 40 obese female patients with type 2 diabetes mellitus. The diabetic females were divided into 2 groups. GI included 20 controlled uncomplicated diabetics & GII included 20 diabetic patients with hypertension and retinopathy. Results: The plasma concentration of adiponectin was significantly lower (P < 0.01) in diabetic females in G & G than non-diabetic control females. In diabetic patients with hypertension and retinopathy ( GII) there was a significant decrease in plasma adiponectin levels (P < 0.01) as compared to their levels in diabetic females in G and control females. Our results also show that there were non-significant changes in plasma resistin in diabetic patients in both groups G & GII as compared to their levels in control group. Conclusion : These results suggest that adiponectin may play a key role in pathophysiology of type 2 diabetes mellitus and its microangiopathy and macrovascular complications.