Molecular and Cellular Endocrinology 2015-08-15

Interleukin-33/ST2 system attenuates aldosterone-induced adipogenesis and inflammation.

Ernesto Martínez-Martínez, Victoria Cachofeiro, Elodie Rousseau, Virginia Álvarez, Laurent Calvier, Amaya Fernández-Celis, Céline Leroy, María Miana, Raquel Jurado-López, Ana M Briones, Frederic Jaisser, Faiez Zannad, Patrick Rossignol, Natalia López-Andrés

文献索引：Mol. Cell. Endocrinol. 411 , 20-7, (2015)

全文：HTML全文

摘要

Interleukin-33 (IL-33) but not soluble ST2 (sST2) exerts anti-inflammatory and protective effects in several tissues. Aldosterone, a proinflammatory mediator which promotes adipogenesis, is elevated in obese patients. The aim of this study was to investigate the interactions between IL-33/ST2 system and Aldosterone in adipose tissue. Rats fed a high fat diet presented increased sST2 expression, diminished IL-33/sST2 ratio and enhanced levels of differentiation and inflammation in adipose tissue as compared to controls. A similar pattern was observed in adipose tissue from C57BL/6 Aldosterone-treated mice. In both animal models, Aldosterone was correlated with sST2. Treatment of 3T3-L1 adipocytes with IL-33 delayed adipocyte differentiation diminished lipid accumulation and decreased inflammation. Aldosterone decreased IL-33 and increased sST2 expressions in differentiated adipocytes. Aldosterone-induced adipocyte differentiation and inflammation were blocked by IL-33 treatment, but sST2 did not exert any effects. The crosstalk between IL-33/ST2 and Aldosterone could be relevant in the metabolic consequences of obesity. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.