Cell Reports
Volume 34, Issue 10, 9 March 2021, 108810
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Phenotypic characterization of Adig null mice suggests roles for adipogenin in the regulation of fat mass accrual and leptin secretion

https://doi.org/10.1016/j.celrep.2021.108810Get rights and content
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Highlights

  • The absence of Adig impairs adipogenesis in vitro

  • High-fat diet (HFD)-induced weight gain is ameliorated in Adig−/− mice

  • Fat-mass-adjusted leptin levels are reduced in Adig−/− mice

  • Leptin secretion is reduced in Adig−/− adipose explants

Summary

Adipogenin (Adig) is an adipocyte-enriched transmembrane protein. Its expression is induced during adipogenesis in rodent cells, and a recent genome-wide association study associated body mass index (BMI)-adjusted leptin levels with the ADIG locus. In order to begin to understand the biological function of Adig, we studied adipogenesis in Adig-deficient cultured adipocytes and phenotyped Adig null (Adig−/−) mice. Data from Adig-deficient cells suggest that Adig is required for adipogenesis. In vivo, Adig−/− mice are leaner than wild-type mice when fed a high-fat diet and when crossed with Ob/Ob hyperphagic mice. In addition to the impact on fat mass accrual, Adig deficiency also reduces fat-mass-adjusted plasma leptin levels and impairs leptin secretion from adipose explants, suggesting an additional impact on the regulation of leptin secretion.

Keywords

adipogenin
adipose tissue
adipogenesis
leptin
knockout mouse

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