1. Phenotypic characterization of Adig null mice suggests roles for adipogenin in the regulation of fat mass accrual and leptin secretion.
- Author
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Alvarez-Guaita A, Patel S, Lim K, Haider A, Dong L, Conway OJ, Ma MKL, Chiarugi D, Saudek V, O'Rahilly S, and Savage DB
- Subjects
- Adipocytes cytology, Adipocytes metabolism, Adipogenesis, Adiponectin genetics, Adiponectin metabolism, Animals, Body Weight, Diet, High-Fat, Female, Glucose Tolerance Test, Leptin blood, Leptin genetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Obese, Nuclear Proteins deficiency, Phenotype, Uncoupling Protein 1 genetics, Uncoupling Protein 1 metabolism, Adipose Tissue metabolism, Leptin metabolism, Nuclear Proteins genetics
- 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., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)- Published
- 2021
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