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Biology subjects

Xu, Y. J.

Publications and source records attributed to Xu, Y. J..

2 recordsLinked to original sources

Quercetin Promotes Adipose Thermogenesis and Metabolic Health

The activation of thermogenesis in brown adipose tissue (BAT) represents a pivotal target for ameliorating disorders of glucose and lipid metabolism. This study sought to elucidate the regulatory effects of quercetin on thermogenesis and glucose-lipid metabolism within brown adipocytes, alongside its underlying molecular mechanisms. The findings demonstrated that quercetin markedly upregulated the expression of uncoupling protein 1 (UCP1), a critical thermogenic protein in brown adipocytes, thereby enhancing cellular thermogenic capacity and effectively mitigating glucose and lipid metabolism disorders. Subsequent mechanistic investigations confirmed that quercetin activated the COX2-PGE2-EP4-UCP1 signaling axis by augmenting the stability of cyclooxygenase 2 (COX2) protein, thus mediating its thermogenic-promoting and metabolism-improving effects. This study identifies quercetin as a potential therapeutic agent for the improvement of glucose and lipid metabolism disorders, uncovers a novel molecular mechanism through which quercetin regulates brown adipocyte thermogenesis, and provides a theoretical and experimental foundation for the application of quercetin in the prevention and treatment of obesity and related metabolic diseases.

molecular biology↗

Cold-activated hepatocyte derived exosomes promote BAT thermogenesis through miR-293-5p

The liver-adipose axis serves as a fundamental regulatory network governing systemic lipid homeostasis, with hepatic-derived signals orchestrating adipose tissue plasticity through multimodal mechanisms. Comprehensive elucidation of these bidirectional crosstalk mechanisms may reveal novel therapeutic strategies for metabolic disorders. Our investigation demonstrates that cold exposure induces hepatic secretion of exosomes that potentiate adipose thermogenic activation in both in vitro and in vivo models. This thermogenic potentiation is mechanistically linked to cold-induced upregulation of hepatocyte-derived exosomal miR-293-5p. Notably, pharmacological administration of miR-293-5p agomir significantly attenuates diet- induced obesity and associated metabolic dysregulation in murine models. Through mechanistic interrogation, we identified Tet1 as a direct downstream target of miR- 293-5p, where ectopic Tet1 expression disrupts brown adipose tissue (BAT) thermogenic programming independently of miR-293-5p modulation. Our findings establish cold-activated hepatocyte exosomes as endocrine signaling mediators containing thermogenic microRNA cargos, with miR-293-5p emerging as a regulatory nexus coordinating mitochondrial bioenergetics and systemic energy equilibrium through liver-adipose cross-talk.

genetics↗