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

Abstract : 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.
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Submitted on : Thursday, March 29, 2018 - 11:52:42 AM
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Ernesto Martinez-Martinez, Victoria Cachofeiro, Elodie Rousseau, Virginia Álvarez, Laurent Calvier, et al.. Interleukin-33/ST2 system attenuates aldosterone-induced adipogenesis and inflammation. Molecular and Cellular Endocrinology, 2015, 411, pp.20 - 27. ⟨10.1016/j.mce.2015.04.007⟩. ⟨hal-01748910⟩



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