AI Article Synopsis
- Glucagon receptor (GCGR) agonism could help reduce liver fat (hepatic steatosis), but the exact mechanism is unclear.
- The protein CD9 is found at lower levels in fatty livers and increases with GCGR activation; it plays a crucial role in managing fat metabolism in the liver.
- Enhancing CD9 levels can improve liver health and reduce fat accumulation, making it a potential target for treating liver fat issues.
Article Abstract
Glucagon receptor (GCGR) agonism offers potentially greater effects on the mitigation of hepatic steatosis. However, its underlying mechanism is not fully understood. Here, it screened tetraspanin CD9 might medicate hepatic effects of GCGR agonist. CD9 is decreased in the fatty livers of patients and upregulated upon GCGR activation. Deficiency of CD9 in the liver exacerbated diet-induced hepatic steatosis via complement factor D (CFD) regulated fatty acid metabolism. Specifically, CD9 modulated hepatic fatty acid synthesis and oxidation genes through regulating CFD expression via the ubiquitination-proteasomal degradation of FLI1. In addition, CD9 influenced body weight by modulating lipogenesis and thermogenesis of adipose tissue through CFD. Moreover, CD9 reinforcement in the liver alleviated hepatic steatosis, and blockage of CD9 abolished the remission of hepatic steatosis induced by cotadutide treatment. Thus, CD9 medicates the hepatic beneficial effects of GCGR signaling, and may server as a promising therapeutic target for hepatic steatosis.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11304330 | PMC |
| http://dx.doi.org/10.1002/advs.202400819 | DOI Listing |
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