ArticleChinese medicine2026
Targeting G-protein-coupled receptors and gut microbiota: Ge-Lian Qi-Shen decoction elevates GLP-1 to combat non-alcoholic fatty liver disease.
Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD), often accompanied by insulin resistance, obesity, and hyperlipidemia, is a challenging metabolic disorder to treat. Ge-Lian Qi-Shen Decoction, a traditional Chinese herbal formula, has been clinically used to alleviate symptoms associated with NAFLD, but its underlying mechanisms remain unclear.
methodsA NAFLD model was established in C57BL/6J mice using a high-fat diet (HFD). The effects of 4-week GQD intervention at different doses on NAFLD-related symptoms were assessed using biochemical analyses, pathological sections, and oral glucose tolerance tests. ELISA and qPCR were employed to investigate the impact of GQD on serum GLP-1 levels and intestinal Gcg gene expression in NAFLD mice. The direct stimulatory effects of GQD on GLP-1 secretion were examined in NCI-H716 cells and HFD-fed mice. UPLC-MS/MS was used to analyze the composition of ileal contents in GQD-treated mice, and the regulatory effects of 24 identified compounds on GLP-1 secretion were evaluated. Additionally, 16S rDNA sequencing, metabolomics and fecal microbiota transplantation were utilized to explore the role of gut microbiota in GQD's anti-NAFLD effect.
resultsGQD improved HFD-induced hepatic steatosis, impaired glucose tolerance, and elevated blood lipid levels in a dose-dependent manner. It increased serum GLP-1 levels, reduced energy intake, and enhanced glucose tolerance in mice. A single dose of GQD directly elevated serum GLP-1 levels in HFD-fed mice and improved glucose tolerance in a GLP-1-dependent manner. In NCI-H716 cells, GQD promoted intracellular calcium influx and GLP-1 release by activating two G-protein-coupled receptors (GPCRs): bitter taste receptors and TGR5. Compounds such as berberine, coptisine, nuciferine, liensinine, higenamine, aurantio-obtusin, and obtusifolin in GQD activated bitter taste receptors, while maslinic acid and cycloastragenol activated TGR5, facilitating GLP-1 secretion. Furthermore, GQD gavage increased the levels of Muribaculaceae and Akkermansia in mouse feces, leading to elevated concentrations of short-chain fatty acids (SCFAs) such as acetate, propionate, butyrate, and valerate. These SCFAs potentially activated fatty acid-related GPCRs, such as GPR41, in the colon, thereby enhancing colonic Gcg expression. FMT experiment showed that gut microbiota can partially mediate the effect of GQD in increasing GLP-1 levels thus alleviating NAFLD.
conclusionSome alkaloids, anthraquinones, and triterpenoids in GQD can activate GPCRs, including bitter taste receptors and TGR5, in intestinal endocrine cells, promoting GLP-1 secretion. Simultaneously, GQD regulates gut microbiota composition and metabolism, increasing SCFA levels and Gcg gene expression, leading to sustained elevation of GLP-1 levels. These combined effects contribute to the alleviation of NAFLD symptoms.
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