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

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

Cell Rep

Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Cambridge, Cambridgeshire CB2 0QQ, UK. Electronic address:

Published: March 2021

AI Article Synopsis

  • - Adipogenin (Adig) is a protein that plays a role in fat cell development and is linked to body mass index (BMI) through genetic studies.
  • - Research involving Adig-deficient fat cells and mice shows that Adig is critical for forming fat cells, with Adig-null mice being leaner than normal ones on a high-fat diet.
  • - The lack of Adig also lowers leptin levels (a hormone related to hunger and fat storage) and affects its secretion from fat tissues, indicating its role in regulating leptin as well.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7966854PMC
http://dx.doi.org/10.1016/j.celrep.2021.108810DOI Listing

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