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

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)20-27
Number of pages8
JournalMolecular and Cellular Endocrinology
StatePublished - Aug 5 2015
Externally publishedYes


  • Adipocyte differentiation
  • Adipose tissue
  • Aldosterone
  • IL-33/ST2 system

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology


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