Lipids & metabolic liver disease
Antagonic effect of ghrelin and LEAP-2 on hepatic stellate cell activation and liver fibrosis in obesity-associated nonalcoholic fatty liver disease
Authors' conclusion
Ghrelin is an anti-fibrogenic factor blocking HSC activation induced by the most potent fibrogenic cytokine, TGF-β1, and LEAP-2. The imbalance between acylated ghrelin and ghrelin receptor antagonist LEAP-2 might contribute to maintain liver fibrosis in patients with obesity and NAFLD.
Study context
- Population
- Patients with severe obesity and nonalcoholic fatty liver disease (NAFLD) with available liver pathology undergoing RYGBcirculating n = 179
- Outcome
- Ghrelin and LEAP-2 vs liver fibrosis and HSC activation
Methodological detailsclinical cohort and in vitro human LX-2 cell experiments
- Clinical cohort and in vitro human LX-2 cell experiments
Main finding
As reported in the abstract
- Plasma and hepatic ghrelin negatively associated with liver fibrosis; LEAP-2 positively associated
- 6 months after RYGB: hepatic function improved; acylated ghrelin and LEAP-2 unchanged, both inversely related to post-surgical TGF-β1 and TIMP-1
- Acylated ghrelin reversed TGF-β1-induced myofibroblast-like phenotype, collagen contractile properties and upregulation of hepatic stellate cell (HSC) activation and fibrogenesis factors via PI3K/Akt/mTOR
- Acylated ghrelin inhibited the mild HSC activation induced by LEAP-2
Original publication
Antagonic effect of ghrelin and LEAP-2 on hepatic stellate cell activation and liver fibrosis in obesity-associated nonalcoholic fatty liver disease. Eur J Endocrinol. Published 26 June 2023. doi:10.
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