Abstract 16726: Brain Natriuretic Peptide Overrides the Effects of Systemic Inflammation and Globally Increases Adiponectin Biosynthesis in Human Adipose Tissue of Patients With Ischaemic Heart Disease
Background: Regulation of adiponectin (AdN) biosynthesis in human adipose tissue (AT) is poorly understood. Pro-inflammatory cytokines suppress AdN expression in cell models, while brain natriuretic peptide (BNP) stimulates its synthesis. We’ve explored the effects of systemic BNP and interleukin-6 (IL-6) on AdN biosynthesis in patients with coronary heart disease (CHD).
Methods: In Study 1, blood samples were collected pre-operatively from 251 patients undergoing cardiac surgery. Femoral (Fem), subcutaneous (Sc) and mesothoracic (Ms) AT samples harvested during operation were incubated ex-vivo for 4h and AdN release was quantified by ELISA. Snap-frozen AT samples were used to determine ADIPOQ gene expression by qRTPCR. Plasma BNP and IL-6 were measured using chemiluminescent- microparticle and enzyme-linked immunoassays respectively. In Study 2, Fem, Sc and Ms AT samples were collected from 11 patients undergoing coronary bypass surgery; these samples were incubated with/without IL-6 (25ng/mL) and tumor necrosis factor-a (4ng/mL) +/- BNP (1nM) for 24h, and changes in AdN release and gene expression were quantified.
Results: Plasma BNP was positively associated with AdN release from all AT depots (A) and circulating AdN levels (B). Plasma IL-6 was inversely associated with AdN release only from Fem-AT (p<0.05) but not from Ms-AT (P=NS) or Sc-AT (P=NS), while BNP reversed the effects of inflammation on AdN released by Fem-AT in the ex-vivo model (C).
Conclusions: Systemic IL-6 suppresses AdN release from Fem-AT but is not a predictor of circulating AdN in CHD patients. BNP is the main driver of plasma AdN in these patients, by globally increasing AdN biosynthesis from all AT depots and overriding the local effects of IL-6 on Fem-AT. These findings provide further insight into the mechanisms of AdN biosynthesis in humans.
- © 2013 by American Heart Association, Inc.