Abstract 154: Differential impact of subcutaneous and visceral adipose tissue derived high molecular weight adiponectin on insulin resistance and type 2 diabetes

Background: Association of visceral adipose tissue (VAT) with high molecular weight (HMW) adiponectin and insulin resistance (IR) is known, whereas impact of subcutaneous adipose tissue (SCAT) is unclear. Our objective was to find out association of VAT and SCAT-derived HMW adiponectin with serum HMW adiponectin and explore their impact on HOMA-IR and type 2 diabetes (T2DM). Methods: Among 51 subjects (Age- 30 to 57 years), 33 subjects (women = 20, men = 13) without T2DM and 18 subjects (women = 11, men = 7) with new onset diabetes (less than 1 year) were categorized as control and T2DM respectively according to American Diabetic Association (ADA) guideline, 2010. Adipocytes were isolated and cultured from adipose tissue biopsies obtained from these subjects during their abdominal surgery. Adiponectin mRNA expression was analysed by Real-Time PCR, and HMW adiponectin secretion were analysed by Enzyme-linked immunosorbent assay (ELISA). Result: In both T2DM and control, no significant changes of adiponectin mRNA expression were found between SCAT and VAT; HMW adiponectin secretion from SCAT was significantly (p = 0.002) higher compared to VAT in both groups. In T2DM group adiponectin mRNA expression and tissue derived HMW adiponectin from SCAT and VAT significantly lower than that of control group. Serum HMW Adiponectin significantly decreased (p < 0.0001) in diabetic group. Spearman correlation analysis showed that, serum HMW adiponectin has stronger positive correlation with SCAT-derived HMW adiponectin (r = 0.51, p < 0.0001) than VAT-derived HMW adiponectin (r = 0.32, p < 0.05). HOMA-IR negatively correlated to serum HMW adiponectin (r = -0.41, p < 0.0001), and more strongly correlated to SCAT-derived HMW adiponectin (r = -0.55, p < 0.0001) than that of VAT (r = -0.42, p < 0.001). Conclusion: HMW adiponectin predominantly secreted from SCAT may exert more impact on circulating HMW adiponectin, thereby leading to increased insulin resistance and risk of T2DM.