Study Of Correlations Between Plasma Obestatin And Relevant Factors In The Different Glucose Tolerances

Objective This study which measureed fasting plasma Obestatin (Obestatin) concentrations of the subjects devided in type 2 diabetes (T2DM),impaired glucose tolerance (IGT) and normal glucose tolerance (NGT) would investigate the relationship between plasma Obestatin and fasting plasma glucose (FPG), 2 hour plasma glucose (2hPG), fasting plasma insulin (FIns), insulin resistance (IR) and plasma lipid as well as other factors in population with different glucose tolerances. Make basic investigations for further understanding the roles of Obestatin in the onset of T2DM and obesity. Working out the effect of Obestatin to glycometabolism disorder, we would hope that a new kind of medicine made from Obestatin or its derivative might come out and be put into clinical application.Methods Plasma Obestatin levels were measured by radioimmunoassay in the patients with type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), and controls (NGT). The relationship between plasma Obestatin levels and BMI, HOMA-IR, plasma glucose, insulin, blood lipids levels were also analyzed by bivariate,and multivariate regression analysis.Results Plasma Obestatin levels in patients with IGT and T2DM were significantly reduced compared with controls (2.41±0.78)ng/ ml and (2.95±0.56)ng/L vs (3.41±0.61)ng/ ml, P 0.01 . Plasma Obestatin levels were also found to be markedly decreased in obese subjects in three groups when compared to subject with BMI 25kg/m2. Plasma Obestatin levels correlated negatively with SBP DBP BMI WHR FPG 2hPG FIns HOMA-IR TG LDL-C CRP (P<0.01 and P<0.05) in simple regression analysis. But in a multiple regression analysis, only BMI and FPG were independently associated with plasma Obestatin levels (P<0.01). In non-obese groupsonly HOMA-IR was independently associated with plasma Obestatin levels(P<0.01).Conclusion The changes of obestatin levels are associated with metabolism disorder, and it may contribute, in part, to the pathogenesis of T2DM.