ArticleDiabetologia2016
JAK2 promotes brown adipose tissue function and is required for diet- and cold-induced thermogenesis in mice.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 47 citations in OpenAlex.
- Chemokine receptor CCR1 restrains adipose tissue remodelling via cAMP/PKA/CREB signalling and adipocyte‒macrophage crosstalk in mice.Clinical and translational medicine · 2026Article
- Cross-Talk Between Signaling and Transcriptional Networks Regulating Thermogenesis-Insights into Canonical and Non-Canonical Regulatory Pathways.International journal of molecular sciences · 2026Review
- Thiamine transporter 2 and Janus kinase 2 inhibitor, fedratinib suppresses thermogenic activation of human neck area-derived adipocytes.Frontiers in endocrinology · 2026Article
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Crosstalk Between Antioxidants and Adipogenesis: Mechanistic Pathways and Their Roles in Metabolic Health.Antioxidants (Basel, Switzerland) · 2025Review
- Spexin ameliorated obesity-related metabolic disorders through promoting white adipose browning mediated by JAK2-STAT3 pathway.Nutrition & metabolism · 2024Article
- Recent advances in JAK inhibitors for the treatment of metabolic syndrome.Frontiers in pharmacology · 2023Review
- Factors Associated with White Fat Browning: New Regulators of Lipid Metabolism.International journal of molecular sciences · 2022Review
- The Mechanism of Leptin on Inhibiting Fibrosis and Promoting Browning of White Fat by Reducing ITGA5 in Mice.International journal of molecular sciences · 2021Article
- Innate-Immunity Genes in Obesity.Journal of personalized medicine · 2021Review
- High expression of CD52 in adipocytes: a potential therapeutic target for obesity with type 2 diabetes.Aging · 2021Article
- Gab2 deficiency suppresses high-fat diet-induced obesity by reducing adipose tissue inflammation and increasing brown adipose function in mice.Cell death & disease · 2021Article
- IFNγ is a Key Link between Obesity and Th1-Mediated AutoImmune Diseases.International journal of molecular sciences · 2020Article
- STAT5 is required for lipid breakdown and beta-adrenergic responsiveness of brown adipose tissue.Molecular metabolism · 2020Article
- The role of microRNA-23b-5p in regulating brown adipogenesis and thermogenic program.Endocrine connections · 2020Article
- Leptin: Is It Thermogenic?Endocrine reviews · 2020Review
- Inflammation and Immunity: From an Adipocyte's Perspective.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019Review
- Nutritional and non-nutritional agents that stimulate white adipose tissue browning.Reviews in endocrine & metabolic disorders · 2019Review
- Identification of a rhodanine derivative BML-260 as a potent stimulator of UCP1 expression.Theranostics · 2019Article
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9 authors at 3 institutions in 2 countries.
Funding
Abstract
aims/hypothesisNon-shivering thermogenesis in adipose tissue can be activated by excessive energy intake or following cold exposure. The molecular mechanisms regulating this activation have not been fully elucidated. The Janus kinase (JAK) - signal transducer and activator of transcription (STAT) pathway mediates the signal transduction of numerous hormones and growth factors that regulate adipose tissue development and function, and may play a role in adaptive thermogenesis.
methodsWe analysed mRNA and protein levels of uncoupling protein 1 (UCP1) and JAK2 in different adipose depots in response to metabolic and thermal stress. The in vivo role of JAK2 in adaptive thermogenesis was examined using mice with adipocyte-specific Jak2 deficiency (A-Jak2 KO).
resultsWe show in murine brown adipose tissue (BAT) that JAK2 is upregulated together with UCP1 in response to high-fat diet (HFD) feeding and cold exposure. In contrast to white adipose tissue, where JAK2 was dispensable for UCP1 induction, we identified an essential role for BAT JAK2 in diet- and cold-induced thermogenesis via mediating the thermogenic response to β-adrenergic stimulation. Accordingly, A-Jak2 KO mice were unable to upregulate BAT UCP1 following a HFD or after cold exposure. Therefore, A-Jak2 KO mice were cold intolerant and susceptible to HFD-induced obesity and diabetes. CONCLUSIONS/
interpretationTaken together, our results suggest that JAK2 plays a critical role in BAT function and adaptive thermogenesis. Targeting the JAK-STAT pathway may be a novel therapeutic approach for the treatment of obesity and related metabolic disorders.
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