Correlation of insulin resistance, beta cell function and insulin sensitivity with serum sFas and sFasL in newly diagnosed type 2 diabetes
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Hemant Kumar, Manish Mishra , Surabhi Bajpa, Deepa Pokhria , Awadhesh Kumar Arya , Rakesh Kumar Singh , Kamlakar Tripathi
- چاپ و سال / کشور: 2011
Description
Pancreatic beta cell dysfunction and reduced insulin sensitivity are fundamental factors associated with glucotoxicity, lipotoxicity and oxidative stress in type 2 diabetic patients (T2DM). Diabetic milieu can induce apoptosis in several types of cells. The aim of present study was to compare circulating soluble apoptotic markers (sFas and sFas-L) with HOMA-IR, HOMA-%S, HOMA-%B in the serum of newly diagnosed T2DM and healthy subjects. For this study, 94 T2DM and 60 healthy subjects were enroled and evaluated for various parameters. Biochemical quantifications were performed with Syncron CX5 autoanalyzer. The levels of serum sFas-L, TNF-a and IL-6 were estimated by flowcytometry. The fasting serum insulin and sFas quantified by ELISA. HOMA-IR, HOMA-%S and HOMA-%B were calculated with HOMA calculator v2.2.2. The levels of TC, TG, LDL-C, VLDL-C were augmented and HDL declined significantly (P\0.001) in diabetics. The levels of serum insulin, TNF-a, IL-6, sFas, HOMA-IR were raised (P\0.001) and sFas-L, HOMA-%S and HOMA-%B were decreased significantly (P\0.001) in T2DM subjects than healthy. In diabetics, serum sFas was positively correlated with HOMA-IR (r = 0.720, P\0.001) and negatively with HOMA-%B (r = -0.642, P\0.001) significantly while serum sFasL was negatively correlated with HOMA-IR (r = -0.483, P\0.001) and positively with HOMA-%B (r = 0.466, P\0.001) significantly. Further, the multivariate stepwise regression analysis shows that HOMA-IR contributes significantly to the variance of sFas and sFasL. Our findings suggest that the pancreatic beta cell dysfunction along with increased insulin resistance appears to be associated with apoptotic markers.
Acta Diabetol DOI 10.1007/s00592-011-0307-8 Received: 4 May 2011 / Accepted: 9 June 2011 Springer-Verlag 201
