Adipocyte-specific IGF1R knockout activates the β-catenin/apelin axis to combat diet-induced obesity in male mice.

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

Abstract (original English)

Aims Obesity, driven by complex genetic and environmental interactions, remains a global health crisis with limited therapeutic options. The insulin-like growth factor 1 receptor (IGF1R) plays dual roles in metabolism and growth, but its tissue-specific functions in adipose biology are controversial. This study investigates how adipose-specific IGF1R knockout impacts systemic metabolism under high-fat diet (HFD) stress and explores the underlying mechanisms. Methods Adipose-specific IGF1R knockout mice (AdIGF1RKO) were generated by crossing Igf1r fl/fl mice with Adipoq-Cre transgenics. Mice were fed a normal chow diet (NCD) or HFD for 20 weeks. Metabolic phenotyping included glucose/insulin tolerance tests, body composition analysis and serum profiling. RNA-seq, Western blot and quantitative real-time reverse transcriptase PCR were used to identify molecular pathways. In vitro studies with stromal vascular fraction (SVF) cells validated β-catenin/apelin interactions. Results AdIGF1RKO male mice exhibited reduced adipose mass under NCD and resisted HFD-induced obesity, showing attenuated hepatic lipid deposition and improved glucose metabolism. Mechanistically, IGF1R knockout enhanced INSR and Akt phosphorylation, driving GSK3β-β-catenin activation and apelin upregulation. Apelin activated AMPK, suppressing lipogenesis and enhancing fatty acid oxidation. Notably, β-catenin's rol

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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