ECE2006 Poster Presentations Diabetes, metabolism and cardiovascular (174 abstracts)
1RIHS, University of Wolverhampton, Wolverhampton, United Kingdom; 2Dept of Biological Sciences, University of Warwick, Coventry, United Kingdom.
Obesity is a risk factor for the metabolic syndrome and type 2 diabetes. Adiponectin, a 30 kDa peptide secreted from adipocytes has been shown to be anti-atherogenic, and anti-inflammatory, as well as affecting insulin resistance and pancreatic beta-cell function. This study investigated the levels of expression of the adiponectin receptor subtypes 1 and 2 (AdR-1 and AdR-2) and regulation of their expression in the pancreatic BRIN-BD11 beta-cells line. Cells were cultured in RPMI-1640 and treated with rosiglitazone (10 micromolar), leptin (10 ng/ml and 50 ng/ml), oleic acid (50 micromolar), palmitic acid (50 micromolar), elaidic acid (50 micromolar) and the PPAR alpha agonist WY14643 (10 micromolar) for 24 hours. Total cellular RNA was extracted and mRNA was assessed by real-time PCR. Expression of AdR- 1 was 30 fold higher than that of AdR-2 (P<0.001) at both low and high glucose concentrations. Rosiglitazione treatment resulted in a 32% decrease in AdR-2 mRNA expression (P=0.029) but had no effect on AdR-1. Oleic acid treatment conversely resulted in a decrease in AdR-1 expression of 28% (P=0.031). Leptin had no effect on expression of either receptor type. These observations confirm the differential expression levels of AdR-1 and -2 in pancreatic beta-cells, and suggest a role for adiponectin in beta-cell function which may be altered in obesity and insulin resistant states.