Capsaicin supplementation modulates the nutrigenomic signature essential for energy metabolism in adipose tissue and liver of bisphenol-A exposed mice.

We investigated how capsaicin supplementation impacts lipid and glucose metabolism in visceral white (vWAT) and brown adipose tissue (BAT) and the liver following exposure to bisphenol A (BPA), a known endocrine disruptor linked with metabolic disorders. qRT-PCR-based gene expression analysis, biochemical estimations in the above tissues, and inflammatory cytokine concentration were performed in vWAT and liver. BPA exposure increased adipose tissue mass and altered the expression of key genes and transcription factors related to glucose and lipid metabolism. Capsaicin supplementation upregulated PPARγ, PGC1α, DIO2, UCP-1, ACOX1, P2rx7, TMEM119, and PRDM16 while downregulating C/EBPα in vWAT of BPA exposed mice. In BAT, it upregulated PPARγ, SREBP, DIO2, UCP-1 and TMEM119. In the liver, it increased PPARγ/α, PGC1α, BMP4, GLUT-2, IRS-1, LeptinR, and SIRT-1 expression while reducing ACC and FOXO-1 expression. Expression of Nrf2 was increased whereas Nlrp3, MCP-1, IL-6, and Nf-kB were downregulated in liver tissues of mice that received capsaicin as a co-treatment with BPA. Alteration in malondialdehyde, nitrite and levels of antioxidants such as GSH and SOD was also prevented by capsaicin supplementation in adipose and liver tissues upon BPA exposure. Further capsaicin supplementation also prevented BPA-induced alteration in IL-1β, IL-6, and TNFα levels in the liver and vWAT. Capsaicin supplementation potentially prevented metabolic disruptions triggered by BPA through targeted adjustments in gene expression within tissues. These findings highlight the role of dietary compounds, such as capsaicin in reducing the impacts of environmental toxins on health.