Endocrine Abstracts (2006) 11 OC30

The release of the adipocytokine visfatin is regulated by glucose and insulin

DG Haider1, G Schaller1, S Kapiotis2, C Maier3, A Luger3 & M Wolzt1

1Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria; 2Institute for Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria; 3Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Background/aim: The novel insulin-mimetic adipocytokine visfatin has been linked to the metabolic syndrome but how the release of the hormone itself is regulated is not characterized yet. The aim of this study was to investigate the effect of different glucose and insulin concentrations on visfatin plasma levels in humans, and to study the involved pathways in vitro in human adipocytes.

Methods: Randomized, double-blind, placebo-controlled crossover study. Three different study days were carried out in nine healthy male subjects (age 26±6 years). Subjects gave informed written consent, and the protocol was approved by the local ethical committee. On each day, systemic glucose concentrations of 5.0, 8.3, and 11.1 mmol/L were attained by stepwise increasing intravenous infusions of glucose, representing fasting and postprandial conditions. Visfatin plasma concentrations were studied during concomitant exogenous hyperinsulinemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control, respectively. Additionally, human adipocytes were cultured to study visfatin release in vitro.

Results: Glucose concentrations of 8.3 mmol/l and 11.1 mmol/l increased circulating visfatin from baseline concentrations of 0.5±0.0 ng/ml to 0.9±0.1 and 2.1±0.3 ng/ml, respectively (P<0.01). Glucose-induced elevation of visfatin was prevented by co-infusion of insulin or somatostatin (P<0.05). Visfatin release from cultured adipocytes was glucose concentration- and time-dependent and involved phosphadityl-inositol-(PI)3-kinase and protein kinase B (AKT) pathways.

Conclusions: Circulating visfatin concentrations are increased by hyperglycaemia. This effect is suppressed by exogenous hyperinsulinemia or somatostatin infusion. Thus, glucose seems to regulate visfatin plasma concentrations. Glucose also regulates visfatin release from cultured human adipocytes; glucose signaling in adipocytes involves the PI3/AKT pathway.

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