ArticleThe Journal of biological chemistry2012
Hepatocyte-specific deletion of Janus kinase 2 (JAK2) protects against diet-induced steatohepatitis and glucose intolerance.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 71 citations in OpenAlex.
- Cathepsin D-driven IL2RG-JAK2 signal hijacking disrupts hepatic insulin action: mechanism-grounded proof that targeting cathepsin D prevents prediabetes.International journal of obesity (2005) · 2026Article
- Adult Growth Hormone Deficiency and Metabolic Dysfunction-Associated Steatotic Liver Disease.Current obesity reports · 2026Review
- Platelet Jak2 deficiency accelerates atherosclerosis with increased inflammatory response.The Journal of biological chemistry · 2025Article
- Geniposide Mitigates Insulin Resistance and Hepatic Fibrosis via Insulin Signaling Pathway.International journal of molecular sciences · 2025Article
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Mechanisms of hesperetin in treating metabolic dysfunction-associated steatosis liver diseaseOpen medicine (Warsaw, Poland) · 2025Article
- GHRH-stimulated pituitary small extracellular vesicles inhibit hepatocyte proliferation and IGF-1 expression by its cargo miR-375-3p.Journal of nanobiotechnology · 2024Article
- USP18 Curbs the Progression of Metabolic Hypertension by Suppressing JAK/STAT Pathway.Cardiovascular toxicology · 2024Article
- Inter-organ metabolic interaction networks in non-alcoholic fatty liver disease.Frontiers in endocrinology · 2024Review
- Growth hormone and nonalcoholic fatty liver disease.Immunometabolism (Cobham, Surrey) · 2023 · on this mapReview
- Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies.International journal of molecular sciences · 2023Review
- Recent advances in JAK inhibitors for the treatment of metabolic syndrome.Frontiers in pharmacology · 2023Review
- Insights into the mechanism of growth and fat deposition by feeding different levels of lipid provided by transcriptome analysis of swamp eel (Frontiers in immunology · 2023Article
- Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Immediate-release tofacitinib reduces insulin resistance in non-diabetic active rheumatoid arthritis patients: A single-center retrospective study.World journal of diabetes · 2022Article
- Therapeutic Effects of Resveratrol on Nonalcoholic Fatty Liver Disease Through Inflammatory, Oxidative Stress, Metabolic, and Epigenetic Modifications.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Flame Retardants-Mediated Interferon Signaling in the Pathogenesis of Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- JAK2-IGF1 axis in osteoclasts regulates postnatal growth in mice.JCI insight · 2021Article
- Dj1 deficiency protects against atherosclerosis with anti-inflammatory response in macrophages.Scientific reports · 2021Article
- Effects of GH/IGF axis on bone and cartilage.Molecular and cellular endocrinology · 2021Review
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is becoming the leading cause of chronic liver disease and is now considered to be the hepatic manifestation of the metabolic syndrome. However, the role of steatosis per se and the precise factors required in the progression to steatohepatitis or insulin resistance remain elusive. The JAK-STAT pathway is critical in mediating signaling of a wide variety of cytokines and growth factors. Mice with hepatocyte-specific deletion of Janus kinase 2 (L-JAK2 KO mice) develop spontaneous steatosis as early as 2 weeks of age. In this study, we investigated the metabolic consequences of jak2 deletion in response to diet-induced metabolic stress. To our surprise, despite the profound hepatosteatosis, deletion of hepatic jak2 did not sensitize the liver to accelerated inflammatory injury on a prolonged high fat diet (HFD). This was accompanied by complete protection against HFD-induced whole-body insulin resistance and glucose intolerance. Improved glucose-stimulated insulin secretion and an increase in β-cell mass were also present in these mice. Moreover, L-JAK2 KO mice had progressively reduced adiposity in association with blunted hepatic growth hormone signaling. These mice also exhibited increased resting energy expenditure on both chow and high fat diet. In conclusion, our findings indicate a key role of hepatic JAK2 in metabolism such that its absence completely arrests steatohepatitis development and confers protection against diet-induced systemic insulin resistance and glucose intolerance.
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