Cidea improves the metabolic profile through expansion of adipose tissue
Gustavo Abreu-Vieira,
Alexander W. Fischer,
Charlotte Mattsson,
Jasper M.A. de Jong,
Irina G. Shabalina,
Mikael Rydén,
Jurga Laurencikiene,
Peter Arner,
Barbara Cannon,
Jan Nedergaard and
Natasa Petrovic ()
Additional contact information
Gustavo Abreu-Vieira: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Alexander W. Fischer: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Charlotte Mattsson: Karolinska Institutet
Jasper M.A. de Jong: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Irina G. Shabalina: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Mikael Rydén: Huddinge, Lipid Laboratory, Karolinska Institutet
Jurga Laurencikiene: Huddinge, Lipid Laboratory, Karolinska Institutet
Peter Arner: Huddinge, Lipid Laboratory, Karolinska Institutet
Barbara Cannon: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Jan Nedergaard: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Natasa Petrovic: Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University
Nature Communications, 2015, vol. 6, issue 1, 1-16
Abstract:
Abstract In humans, Cidea (cell death-inducing DNA fragmentation factor alpha-like effector A) is highly but variably expressed in white fat, and expression correlates with metabolic health. Here we generate transgenic mice expressing human Cidea in adipose tissues (aP2-hCidea mice) and show that Cidea is mechanistically associated with a robust increase in adipose tissue expandability. Under humanized conditions (thermoneutrality, mature age and prolonged exposure to high-fat diet), aP2-hCidea mice develop a much more pronounced obesity than their wild-type littermates. Remarkably, the malfunctioning of visceral fat normally caused by massive obesity is fully overcome—perilipin 1 and Akt expression are preserved, tissue degradation is prevented, macrophage accumulation is decreased and adiponectin expression remains high. Importantly, the aP2-hCidea mice display enhanced insulin sensitivity. Our data establish a functional role for Cidea and suggest that, in humans, the association between Cidea levels in white fat and metabolic health is not only correlative but also causative.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8433
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DOI: 10.1038/ncomms8433
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