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dc.contributor.author
Leiss, Veronika
dc.contributor.author
Schönsiegel, Annika
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Gnad, Thorsten
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Kerner, Johannes
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Kaur, Jyotsna
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Sartorius, Tina
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Machann, Jürgen
dc.contributor.author
Schick, Fritz
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Häring, Hans Ulrich
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Pfeifer, Alexander
dc.contributor.author
Nürnberg, Bernd
dc.date.available
2021-09-17T11:19:06Z
dc.date.issued
2020-10
dc.identifier.citation
Leiss, Veronika; Schönsiegel, Annika; Gnad, Thorsten; Kerner, Johannes; Kaur, Jyotsna; et al.; Lack of Gαi2 proteins in adipocytes attenuates diet-induced obesity; Elsevier; Molecular Metabolism; 40; 10-2020; 1-13
dc.identifier.issn
2212-8778
dc.identifier.uri
http://hdl.handle.net/11336/140621
dc.description.abstract
Objectives: Typically, obesity results from an inappropriate balance between energy uptake from nutrient consumption and burning of calories, which leads to a pathological increase in fat mass. Obesity is a major cause of insulin resistance and diabetes. Inhibitory G proteins (Gαi) form a subfamily that is involved in the regulation of adipose tissue function. Among the three Gαi members, i.e. Gαi1, Gαi2, Gαi3, the Gαi2, protein is predominantly expressed in adipose tissue. However, the functions of the Gαi2 isoform in adipose tissue and its impact on the development of obesity are poorly understood. Methods: By using AdipoqCreERT2 mice, we generated adipocyte-specific Gnai2-deficient mice to study Gαi2 function, specifically in white and brown adipocytes. These mice were fed either a control diet (CD) or a high fat diet (HFD). Mice were examined for obesity development, insulin resistance and glucose intolerance. We examined adipocyte morphology and the development of inflammation in the white adipose tissue. Finally, intracellular cAMP levels as an indicator of Gαi signaling and glycerol release as an indicator of lipolysis rates were measured to verify the impact of Gαi2 on the signaling pathway in brown and white adipocytes. Results: An adipocyte-specific deficiency of Gαi2 significantly reduced diet-induced obesity, leading to decreased fat masses, smaller adipocytes and decreased inflammation in the white adipose tissue relative to littermate controls. Concurrently, oxygen consumption of brown adipocytes and in vivo measured energy expenditure were significantly enhanced. In addition, glucose tolerance and insulin sensitivity of HFD-fed adipocyte-specific Gnai2-deficient mice were improved compared to the respective controls. In the absence of Gαi2, adrenergic stimulation of intracellular adipocyte cAMP levels was increased, which correlated with increased lipolysis and energy expenditure. Conclusion: We conclude that adipocyte Gαi2 is a major regulator of adipocyte lipid content in diet-induced obesity by inhibiting adipocyte lipolysis in a cAMP-dependent manner resulting in increased energy expenditure.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
ADIPOCYTES
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BROWN ADIPOSE TISSUE
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G PROTEINS
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GNAI2
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HIGH FAT DIET
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INSULIN
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OBESITY
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WHITE ADIPOSE TISSUE
dc.subject.classification
Biología Celular, Microbiología
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Lack of Gαi2 proteins in adipocytes attenuates diet-induced obesity
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2021-09-15T15:15:18Z
dc.journal.volume
40
dc.journal.pagination
1-13
dc.journal.pais
Alemania
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dc.description.fil
Fil: Leiss, Veronika. Eberhard Karls Universität Tübingen; Alemania
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Fil: Schönsiegel, Annika. Eberhard Karls Universität Tübingen; Alemania
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Fil: Gnad, Thorsten. Universitat Bonn; Alemania
dc.description.fil
Fil: Kerner, Johannes. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Kaur, Jyotsna. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Sartorius, Tina. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Machann, Jürgen. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Schick, Fritz. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
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Fil: Häring, Hans Ulrich. Eberhard Karls Universität Tübingen; Alemania
dc.description.fil
Fil: Pfeifer, Alexander. Universitat Bonn; Alemania
dc.description.fil
Fil: Nürnberg, Bernd. Eberhard Karls Universität Tübingen; Alemania
dc.journal.title
Molecular Metabolism
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.molmet.2020.101029
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S2212877820301034?via%3Dihub
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