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Identification of fatty acid binding protein 4 as an adipokine that regulates insulin secretion during obesity

Abstract

A critical feature of obesity is enhanced insulin secretion from pancreatic beta-cells, enabling the majority of individuals to maintain glycaemic control despite adiposity and insulin resistance. Surprisingly, the factors coordinating this adaptive beta-cell response with adiposity have not been delineated. Here we show that fatty acid binding protein 4 (FABP4/aP2) is an adipokine released from adipocytes under obesogenic conditions, such as hypoxia, to augment insulin secretion. The insulinotropic action of FABP4 was identified using an in vitro system that recapitulates adipocyte to beta-cell endocrine signalling, with glucose-stimulated insulin secretion (GSIS) as a functional readout, coupled with quantitative proteomics. Exogenous FABP4 potentiated GSIS in vitro and in vivo, and circulating FABP4 levels correlated with GSIS in humans. Insulin inhibited FABP4 release from adipocytes in vitro, in mice and in humans, consistent with feedback regulation. These data suggest that FABP4 and insulin form an endocrine loop coordinating the beta-cell response to obesity.

Type Journal
ISBN 2212-8778 (Electronic) 2212-8778 (Linking)
Authors Wu, L. E.; Samocha-Bonet, D.; Whitworth, P. T.; Fazakerley, D. J.; Turner, N.; Biden, T. J.; James, D. E.; Cantley, J.;
Garvan Authors Dr Dorit Samocha-Bonet , Dr Nigel Turner , Prof Trevor Biden
Publisher Name Molecular Metabolism
Published Date 2014-01-01 00:00:00
Published Volume 3
Published Issue 4
Published Pages 465-73
URL http://www.ncbi.nlm.nih.gov/pubmed/24944906
Status Published In-print
OpenAccess Link https://publications.gimr.garvan.org.au/download.php?12490_12868/14_Wu_MM_.pdf