Cell Reports (Mar 2021)

Phenotypic characterization of Adig null mice suggests roles for adipogenin in the regulation of fat mass accrual and leptin secretion

  • Anna Alvarez-Guaita,
  • Satish Patel,
  • Koini Lim,
  • Afreen Haider,
  • Liang Dong,
  • Olivia J. Conway,
  • Marcella K.L. Ma,
  • Davide Chiarugi,
  • Vladimir Saudek,
  • Stephen O’Rahilly,
  • David B. Savage

Journal volume & issue
Vol. 34, no. 10
p. 108810

Abstract

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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.

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