ArticleScientific reports2020
Dipeptidyl peptidase-4 inhibition prevents nonalcoholic steatohepatitis-associated liver fibrosis and tumor development in mice independently of its anti-diabetic effects.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 72 citations in OpenAlex.
- Incretin and Glucagon Signalling in MASLD and MASH: Integrating Metabolic Pathways With Disease Progression.Diabetes, obesity & metabolism · 2026Review
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Gemigliptin Alleviates Succinate Induced Endoplasmic Reticulum Stress and Activation of Hepatic Stellate Cells.Journal of Korean medical science · 2025Article
- Chemoprevention of hepatocellular carcinoma.Hepatology communications · 2025Review
- Association of GLP1-Receptor Agonists with Risk of Hepatocellular Carcinoma: A Retrospective Cohort Study.Drug safety · 2025Article
- DPP4-inhibition reduces pro-inflammatory cytokine production by alpha-beta and gamma-delta T cells in vitro and in the biliary atresia mouse model.Scientific reports · 2025Article
- Glucagon-like peptide 1 receptor agonists and cancer risk: advancing precision medicine through mechanistic understanding and clinical evidence.Biomarker research · 2025 · on this mapReview
- Dipeptidyl peptidase-4 enzyme inhibition and its impacts on hepatic preneoplasia: a new avenue for liver cancer management.Frontiers in pharmacology · 2025Article
- MAFLD: an optimal framework for understanding liver cancer phenotypes.Journal of gastroenterology · 2023Review
- Long-term efficacy and safety of early alogliptin initiation in subjects with type 2 diabetes: an extension of the SPEAD-A study.Scientific reports · 2023Observational
- Pharmacotherapies of NAFLD: updated opportunities based on metabolic intervention.Nutrition & metabolism · 2023Review
- Porphyromonas gingivalis-odontogenic infection is the potential risk for progression of nonalcoholic steatohepatitis-related neoplastic nodule formation.Scientific reports · 2023Article
- Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, modulates glucose production, and when absent influences NAFLD progression.JCI insight · 2023Article
- Medium-chain fatty acids suppress lipotoxicity-induced hepatic fibrosis via the immunomodulating receptor GPR84.JCI insight · 2023Article
- Novel Therapeutic Potentials of Taxifolin for Obesity-Induced Hepatic Steatosis, Fibrogenesis, and Tumorigenesis.Nutrients · 2023Article
- Mechanisms of tumor-associated macrophages affecting the progression of hepatocellular carcinoma.Frontiers in pharmacology · 2023Review
- Immunotherapy for NAFLD and NAFLD-related hepatocellular carcinoma.Frontiers in endocrinology · 2023Review
- Serum protein biomarkers for HCC risk prediction in HIV/HBV co-infected people: a clinical proteomic study using mass spectrometry.Frontiers in immunology · 2023Article
- Gemigliptin Alleviates Succinate-Induced Hepatic Stellate Cell Activation by Ameliorating Mitochondrial Dysfunction.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Mesenchymal stromal cells in the thymus.Inflammation and regeneration · 2022Review
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Authors and funding
20 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH) is a hepatic phenotype of the metabolic syndrome, and increases the risk of cirrhosis and hepatocellular carcinoma (HCC). Although increasing evidence points to the therapeutic implications of certain types of anti-diabetic agents in NASH, it remains to be elucidated whether their effects on NASH are independent of their effects on diabetes. Genetically obese melanocortin 4 receptor-deficient (MC4R-KO) mice fed Western diet are a murine model that sequentially develops hepatic steatosis, NASH, and HCC in the presence of obesity and insulin resistance. In this study, we investigated the effect of the dipeptidyl peptidase-4 (DPP-4) inhibitor anagliptin on NASH and HCC development in MC4R-KO mice. Anagliptin treatment effectively prevented inflammation, fibrosis, and carcinogenesis in the liver of MC4R-KO mice. Interestingly, anagliptin only marginally affected body weight, systemic glucose and lipid metabolism, and hepatic steatosis. Histological data and gene expression analysis suggest that anagliptin treatment targets macrophage activation in the liver during the progression from simple steatosis to NASH. As a molecular mechanism underlying anagliptin action, we showed that glucagon-like peptide-1 suppressed proinflammatory and profibrotic phenotypes of macrophages in vitro. This study highlights the glucose metabolism-independent effects of anagliptin on NASH and HCC development.
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