Horm Metab Res 2007; 39(12): 915-918
DOI: 10.1055/s-2007-993156
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Effects of Spironolactone on Glucose Transport and Interleukin-6 Secretion in Adipose Cells of Women

A. Corbould 1
  • 1Prince Henry's Institute of Medical Research, Clayton, VIC, Australia
Further Information

Publication History

received 18.12.2006

accepted 18.06.2007

Publication Date:
13 December 2007 (online)

Abstract

Adipose tissue inflammation and insulin resistance are central to the pathogenesis of the metabolic syndrome. Spironolactone, an antagonist of mineralocorticoid receptor, glucocorticoid receptor and androgen receptor, and agonist of progesterone receptor, has anti-inflammatory activity. Blockade of the renin-angiotensin-aldosterone system has been shown to improve glucose metabolism. We have investigated whether spironolactone has direct effects on glucose uptake and interleukin-6 secretion in human adipocytes. Spironolactone, but not its active metabolite canrenoic acid, significantly increased basal and insulin-stimulated glucose uptake in cultured in vitro-differentiated adipocytes of women, without affecting insulin sensitivity. The effect was not due to changes in abundance of glucose transporters 1 or 4 or in degree of cell differentiation. Spironolactone, but not canrenoic acid, significantly reduced basal interleukin-6 secretion by cultured stromal-vascular cells. These effects of spironolactone were not mediated by ligand-dependent antagonism of the mineralocorticoid, glucocorticoid, or androgen receptors. Spironolactone may have a novel role in increasing glucose uptake into adipose cells and attenuating adipose tissue inflammation, with implications for management of metabolic syndrome.

References

Correspondence

A. Corbould, MBBS Hons, PhD, FRACP 

Prince Henry's Institute of Medical Research

Block E, Level 4

Monash Medical Centre

Clayton Road

Clayton

3168 VIC

Australia

Phone: +61/395/94 30 07

Fax: +61/395/94 61 25

Email: [email protected]

Email: [email protected]