Abstract
SummaryAdipogenin (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.
Highlights
Adipogenin (Adig) known as SMAF1, for Small Adipocyte Factor 1, is a small (~10 kDa) membrane protein (Hong et al, 2005; Kim et al, 2005)
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 adipogenin, we studied adipogenesis in Adig deficient cultured adipocytes and phenotyped Adig null (Adig-/-) mice
Summary
Adipogenin (Adig) known as SMAF1, for Small Adipocyte Factor 1, is a small (~10 kDa) membrane protein (Hong et al, 2005; Kim et al, 2005). The GWAS performed by Kilpeläinen et al involved data from 32,161 individuals and suggested that a SNP (rs6071166) near the SLC32A1 locus was associated with BMI-adjusted leptin concentrations. The SNP was not associated with mRNA expression of nearby genes in AT, liver, lymphocytes, brain or skin, the authors measured the expression levels of murine homologous genes surrounding the variant in mouse AT. This analysis identified Adig as a candidate gene in the SLC32A1 locus as it was relatively highly expressed compared to other nearby genes. Knockdown of Adig in epididymal AT explants decreased leptin expression and secretion by ~25% (Kilpelainen et al, 2016)
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