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Resolution of NASH and hepatic fibrosis by the GLP-1R and GCGR dual-agonist cotadutide via modulating mitochondrial function and lipogenesis
Cotadutide may improve fatty liver disease and liver scarring by affecting energy use and fat production in liver cells
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Abstract
Cotadutide significantly reduced liver fibrosis in preclinical mouse models of non-alcoholic steatohepatitis (NASH) compared to Liraglutide or Obeticholic acid.
- Cotadutide reduces body weight, food intake, and improves glucose control primarily through GLP-1 signaling.
- The reduction of liver lipid content and enhancement of mitochondrial function is directly mediated by Gcg signaling.
- Key enzymes involved in lipid and glucose metabolism in the liver show specific phosphorylation changes in response to Cotadutide treatment.
- Metabolomic and transcriptomic analyses indicate involvement of lipogenic, fibrotic, and inflammatory pathways associated with Gcg receptor activation.
- The therapeutic effects of Cotadutide suggest a multi-faceted approach to improve liver function in steatohepatitis.
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