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

Adig 基因缺失小鼠的表型表征表明脂肪生成素在调节脂肪量累积和瘦素分泌中发挥作用

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作者: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

Abstract

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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