Adiponectin expression is induced by vitamin E via a peroxisome proliferator-activated receptor γ-dependent mechanism

Abstract

Adiponectin is a well-known adipokine secreted by adipocytes that presents insulin-sensitizing properties. The regulation of expression of this adipokine by micronutrients is largely unknown. We demonstrate here that adiponectin expression is induced in adipocytes after exposure to tocopherols via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. Vitamin E force feeding resulted in an induction of adiponectin in mice at both mRNA and protein levels. Adiponectin mRNA and protein secretion were also increased by vitamin E (α- and γ-tocopherol) in 3T3-L1 cells, together with PPARγ mRNA, independent of an antioxidant effect. In transient transfections, both α-and γ-vitamers induced the luciferase gene reporter under the control of a human adiponectin promoter via a PPAR-responsive element. The induction of adiponectin by tocopherols seems to be PPARγ dependent, because it was blocked by the specific antagonist GW9662. Finally, we showed that intracellular concentrations of a PPARγ endogenous ligand, 15-deoxy-Δ12,14-prostaglandin J2, increased after treatment with tocopherols in 3T3-L1 cells. In summary, vitamin E up-regulates adiponectin expression via a mechanism that implicates PPARγ together with its endogenous ligand 15-deoxy-Δ12,14-prostaglandin J2. The induction of adiponectin via an original molecular mechanism could be considered as the basis for the beneficial effect of vitamin E on insulin sensitivity. Copyright © 2009 by The Endocrine Society.