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Genistein-mediated thermogenesis and white-to-beige adipocyte differentiation involve transcriptional activation of cAMP response elements in the Ucp1 promoter. | LitMetric

AI Article Synopsis

  • Genistein, a bioactive isoflavone found in soybeans, activates thermogenesis in fat tissue of rats and mice, enhancing energy dissipation in response to various conditions like cold and a high-fat diet.
  • The study specifically investigates how genistein influences the expression of uncoupling protein 1 (UCP1), a key player in heat generation within brown and beige fat cells.
  • Results show that genistein increases UCP1 levels through a mechanism involving binding of the CREB protein to the UCP1 promoter, identifying potential applications for genistein in treating metabolic disorders.

Article Abstract

Genistein is an isoflavone present in soybeans and is considered a bioactive compound due to its widely reported biological activity. We have previously shown that intraperitoneal genistein administration and diet supplementation activates the thermogenic program in rats and mice subcutaneous white adipose tissue (scWAT) under multiple environmental cues, including cold exposure and high-fat diet feeding. However, the mechanistic insights of this process were not previously unveiled. Uncoupling protein 1 (UCP1), a mitochondrial membrane polypeptide responsible for dissipating energy into heat, is considered the most relevant thermogenic marker; thus, we aimed to evaluate whether genistein regulates UCP1 transcription. Here we show that genistein administration to thermoneutral-housed mice leads to the appearance of beige adipocyte markers, including a sharp upregulation of UCP1 expression and protein abundance in scWAT. Reporter assays showed an increase in UCP1 promoter activity after genistein stimulation, and in silico analysis revealed the presence of estrogen (ERE) and cAMP (CRE) response elements as putative candidates of genistein activation. Mutation of the CRE but not the ERE reduced genistein-induced promoter activity by 51%. Additionally, in vitro and in vivo ChIP assays demonstrated the binding of CREB to the UCP1 promoter after acute genistein administration. Taken together, these data elucidate the mechanism of genistein-mediated UCP1 induction and confirm its potential applications in managing metabolic disorders.

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Source
http://dx.doi.org/10.1096/fj.202300139RRDOI Listing

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