ABSTRACT: Obesity is a major risk factor for insulin resistance, type 2 diabetes, heart disease, and many other chronic diseases The current study was designed to investigate the endogenous mechanism by which obesity may increase
the risk of CVD by examining whether serum adiponectin, Leptin or insulin mediate the association of obesity and type2 diabetes and cardiovascular risk factors in Egyptian adult patients. Patients and Methods: This study included 82 subjects, 30 patients suffering from type 2 diabetes and 52 patients suffering from type 2 diabetes together with coronary artery disease (CAD) together with another group having CAD without diabetes. They were classified according to their body mass index (BMI) into obese and non-obese groups, also 25 healthy volunteers were considered as controls. All patients were subjected to anthropometric assessment and laboratory determination of serum Adiponectin, Leptin, insulin and glucose. Insulin resistance was established by homeostasis model assessment (HOMA-IR) Differences in clinical or laboratory parameters among groups were compared by using one-way ANOVA test. Results revealed highly significant decrease in Adiponectin levels and highly significant increase in serum Leptin in non obese groups (G1 (T2D), G2 (CAD) and G3 (T2D+ CAD) as compared to controls. However, there were no statistical variations between non obese groups when compared to each others. HOMA-IR
showed highly significant increase in non obese groups as compared to both controls and each other. Also, the results showed high significant decrease in Adiponectin and highly significant increase in Leptin in obese groups
(G4 (T2D), G5 (CAD) and G6 (T2D+CAD) when compared to controls. However, there were no statistical
variations between obese groups when compared to each others as regard Adiponectin, while Leptin showed statistical increase between (G4) and (G5) groups when compared to each others, HOMA-IR showed highly
significant increase in the two obese groups only (G4 and G6) as compared to controls, while there was no significant variation in (G5) when compared to controls. Moreover, there was a significant increase in all obese groups when compared to each other. Also, there was significant correlation between serum Adiponectin and Leptin in obese DM patients. Conclusion: The coexistence of correlation between serum leptin and Adiponectin levels in addition to increase of serum leptin and decrease serum Adiponectin levels in obese DM patients in the current study; support the hypothesis of their susceptibility to atherosclerosis.
Journal of American Science. 01/2010; 6.