Schisantherin A interacts with gut bacteria to stimulate adipose tissue thermogenesis in obese mice via a TGR5‒p-CREB‒STAT6 signaling pathway

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The global epidemic of obesity challenges the scientific and medical communities to find different treatments. Schisantherin A (Sin A), a natural compound isolated from Schisandra chinensis (Turcz.), reduces the abundance of bile salt hydrolase-producing gut bacteria in obese mice, leading to accumulation of specific conjugated bile acids (CBAs). These elevated CBAs activate a signaling axis containing Takeda G protein-coupled receptor 5, phosphorylated cAMP-responsive element binding protein 1, and signal transducer and activator of transcription 6 (TGR5-p-CREB-STAT6), wherein CREB directly binds to the STAT6 promoter. Sin A-induced STAT6 activation promoted M2-like macrophages polarization to secret slit guidance ligand 3 (SLIT3), which consequently stimulated norepinephrine release in sympathetic neurons and induced thermogenesis in adipose tissue. This study thus identifies a pathway by which Sin A interacts with gut bacteria to stimulate CBA-mediated beiging of white adipose tissue, highlighting a promising natural product-based strategy for obesity treatment.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.