MIF tautomerase inhibitor 4-IPP alleviates HFD-induced obesity by restoring CD137-mediated browning of white adipocytes in mice.
Chen CJ., Guo DW., Yuan QY., Zhuo YQ., Yang SF., Xu HM.
Animal Study, published in Acta Pharmacol Sin (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Acta Pharmacol Sin (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41741765
- DOI
- 10.1038/s41401-026-01755-3
Abstract (original English)
Macrophage migration inhibitory factor (MIF) is a cytokine that possesses multiple enzymatic activities, such as keto-enol tautomerase and thiol-oxidoreductase. We previously found that lack of MIF tautomerase activity significantly alleviated high fat diet (HFD)-induced obesity in mice. In this study, we investigated the regulatory mechanisms of MIF tautomerase in obesity. HFD-induced obese mouse model was established. Adipogenic differentiation was induced in mouse preadipocyte cell line 3T3-L1 and mouse adipose-derived mesenchymal stem cells (ADSCs) in vitro. We showed that MIF tautomerase inhibitors ISO-1 or 4-IPP dose-dependently promoted lipid degradation and mitochondrial thermogenesis by enhancing basal oxygen consumption rate and proton leak, accompanied by increased expression of browning markers (UCP1, PGC-1α, DIO2, CD137) in 3T3-L1 cells under adipogenic induction conditions. In HFD-induced obese mice, administration of 4-IPP (5, 10 mg/kg, i.p.) every 2 days for 12 weeks significantly ameliorated HFD-induced obesity, improved insulin sensitivity, and enhanced energy expenditure. In white adipocytes, 4-IPP (1, 5, 10 μM) dose-dependently promoted CD137 expression, and restored CD137-mediated activation of the PI3K/AKT signaling to improve lipid metabolism. CD137 deficiency abrogated the browning effect of 4-IPP in white adipocytes in vitro. CD137 -/- mice exhibited in
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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