Disruption of the circadian clock component BMAL1 elicits an endocrine adaption impacting on insulin sensitivity and liver disease.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
08 03 2022
Historique:
entrez: 3 3 2022
pubmed: 4 3 2022
medline: 22 3 2022
Statut: ppublish

Résumé

SignificanceWhile increasing evidence associates the disruption of circadian rhythms with pathologic conditions, including obesity, type 2 diabetes, and nonalcoholic fatty liver diseases (NAFLD), the involved mechanisms are still poorly described. Here, we show that, in both humans and mice, the pathogenesis of NAFLD is associated with the disruption of the circadian clock combined with perturbations of the growth hormone and sex hormone pathways. However, while this condition protects mice from the development of fibrosis and insulin resistance, it correlates with increased fibrosis in humans. This suggests that the perturbation of the circadian clock and its associated disruption of the growth hormone and sex hormone pathways are critical for the pathogenesis of metabolic and liver diseases.

Identifiants

pubmed: 35238641
doi: 10.1073/pnas.2200083119
pmc: PMC8916004
doi:

Substances chimiques

ARNTL Transcription Factors 0
BMAL1 protein, human 0
Leptin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2200083119

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Auteurs

Céline Jouffe (C)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
Department of Pharmacology and Toxicology, University of Lausanne, CH-1011 Lausanne, Switzerland.
Helmholtz Diabetes Center, Helmholtz Zentrum München, DE-85764 Neuherberg, Germany.

Benjamin D Weger (BD)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
Institute for Molecular Bioscience, The University of Queensland, St. Lucia QLD 4072, Australia.

Eva Martin (E)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.

Florian Atger (F)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
Department of Pharmacology and Toxicology, University of Lausanne, CH-1011 Lausanne, Switzerland.

Meltem Weger (M)

Institute for Molecular Bioscience, The University of Queensland, St. Lucia QLD 4072, Australia.

Cédric Gobet (C)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
School of Life Sciences, École Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.

Divya Ramnath (D)

Institute for Molecular Bioscience, The University of Queensland, St. Lucia QLD 4072, Australia.

Aline Charpagne (A)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.

Delphine Morin-Rivron (D)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.

Elizabeth E Powell (EE)

Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane QLD 4102, Australia.
Faculty of Medicine, Center for Liver Disease Research, Translational Research Institute, The University of Queensland, Brisbane QLD 4102, Australia.

Matthew J Sweet (MJ)

Institute for Molecular Bioscience, The University of Queensland, St. Lucia QLD 4072, Australia.

Mojgan Masoodi (M)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
Institute of Clinical Chemistry, Bern University Hospital, Bern 3010, Switzerland.

N Henriette Uhlenhaut (NH)

Helmholtz Diabetes Center, Helmholtz Zentrum München, DE-85764 Neuherberg, Germany.
Metabolic Programming, Technical University of Munich School of Life Sciences, DE-85354 Freising, Germany.

Frédéric Gachon (F)

Nestlé Research, Société des Produits Nestlé, CH-1015 Lausanne, Switzerland.
Institute for Molecular Bioscience, The University of Queensland, St. Lucia QLD 4072, Australia.
School of Life Sciences, École Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.

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Classifications MeSH