ArticleScientific reports2026
SOCS1-based therapeutic peptides improve liver disease and metabolic dysfunction in obesity and diabetes.
Article in Scientific reports, 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
Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a growing global health challenge, closely linked to obesity and type 2 diabetes mellitus. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is a key mediator of inflammation and metabolic dysregulation in liver disease. This study investigates the therapeutic potential of a SOCS1-derived peptidomimetic (MiS1) in a mouse model of MASLD using obese, type 2 diabetic BTBR ob/ob mice. A six-week treatment with MiS1 (10 μg/g/day) significantly reduced body weight, serum transaminase levels, hepatic steatosis, and hepatocellular ballooning compared to untreated controls. MiS1-treated mice exhibited decreased hepatic triglyceride content, notably in palmitic (C16:0) and palmitoleic (C16:1n-7) acids, along with downregulation of key lipogenic enzymes. Inflammatory signaling was also attenuated, with lower expression of pro-inflammatory cytokines and increased expression of CD163, a marker of M2 anti-inflammatory macrophages. In vitro, MiS1 directly inhibited insulin-induced STAT3 phosphorylation and suppressed lipogenic gene expression in murine hepatocytes. These results demonstrate that JAK/STAT pathway inhibition via MiS1 ameliorates key pathological features of MASLD by concurrently targeting hepatic lipid metabolism and inflammation, highlighting its potential as a novel therapeutic approach for patients with obesity and diabetes.
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