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Metabolic homeostasis is maintained by the coordinated action of multiple organ systems. Insulin secretion is often enhanced during obesity or insulin resistance to maintain glucose and lipid homeostasis, whereas a loss of insulin secretion is associated with type 2 diabetes. Adipocytes secrete hormones known as adipokines which act on multiple cell types to regulate metabolism. Many adipokines have been shown to influence beta cell function by enhancing or inhibiting insulin release or by influencing beta cell survival. Insulin, in turn, regulates lipolysis and promotes glucose uptake and lipid storage in adipocytes. As adipokine secretion and action is strongly influenced by obesity, this provides a potential route by which beta cell function is coordinated with adiposity, independently of alterations in blood glucose or lipid levels. In this review, I assess the evidence for the direct regulation of beta cell function by the adipokines leptin, adiponectin, extracellular nicotinamide phosphoribosyltransferase, apelin, resistin, retinol binding protein 4, fibroblast growth factor 21, nesfatin-1 and fatty acid binding protein 4. I summarise in vitro and in vivo data and discuss the influence of obesity and diabetes on circulating adipokine concentrations, along with the potential for influencing beta cell function in human physiology. Finally, I highlight future research questions that are likely to yield new insights into the exciting field of insulinotropic adipokines.

Original publication

DOI

10.1007/s00335-014-9538-7

Type

Journal article

Journal

Mamm Genome

Publication Date

10/2014

Volume

25

Pages

442 - 454

Keywords

Adipocytes, Adipokines, Adiponectin, Animals, Calcium-Binding Proteins, DNA-Binding Proteins, Fatty Acid-Binding Proteins, Fibroblast Growth Factors, Homeostasis, Humans, Insulin, Insulin-Secreting Cells, Leptin, Nerve Tissue Proteins, Nicotinamide Phosphoribosyltransferase, Resistin, Retinol-Binding Proteins, Plasma, Signal Transduction