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

Alvarez-Guaita, A., Patel, S., Lim, K., Haider, A., Dong, L., Conway, O. J., et al. (2021). Phenotypic characterization of Adig null mice suggests roles for adipogenin in the regulation of fat mass accrual and leptin secretion. Cell Reports, 34(10): 108810. doi:10.1016/j.celrep.2021.108810.

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 Creators:
Alvarez-Guaita, Anna1, Author
Patel, Satish1, Author
Lim, Koini1, Author
Haider, Afreen1, Author
Dong, Liang1, Author
Conway, Olivia J.1, Author
Ma, Marcella K.L.1, Author
Chiarugi, Davide2, Author           
Saudek, Vladimir1, Author
O’Rahilly, Stephen1, Author
Savage, David B.1, Author
Affiliations:
1External Organizations, ou_persistent22              
2Methods and Development Group Computing and Databases Services, MPI for Human Cognitive and Brain Sciences, Max Planck Society, ou_2205651              

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Free keywords: Adipogenin; Adipose tissue; Adipogenesis; Leptin; Knockout mouse
 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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Language(s): eng - English
 Dates: 2020-12-232020-05-042021-02-092021-03-09
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.1016/j.celrep.2021.108810
PMID: 33691105
PMC: PMC7966854
 Degree: -

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Project name : -
Grant ID : 4050678413
Funding program : -
Funding organization : UK Research & Innovation (UKRI)
Project name : -
Grant ID : -
Funding program : -
Funding organization : National Institutes of Health (NIH)
Project name : -
Grant ID : WT 107064; 208363/Z/17/Z
Funding program : -
Funding organization : Wellcome Trust
Project name : -
Grant ID : MRC_MC_UU_12012.1; MC_UU_00014/5
Funding program : -
Funding organization : Medical Research Council UK (MRC)
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Grant ID : -
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Funding organization : NIHR Rare Disease Translational Research Collaboration
Project name : Cambridge Biomedical Research Centre
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Funding program : -
Funding organization : National Institutes for Health Research (NIHR)

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Title: Cell Reports
Source Genre: Journal
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Publ. Info: Maryland Heights, MO : Cell Press
Pages: - Volume / Issue: 34 (10) Sequence Number: 108810 Start / End Page: - Identifier: ISSN: 2211-1247
CoNE: https://pure.mpg.de/cone/journals/resource/2211-1247