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Jouffe, C. ; Weger, B.D.* ; Martin, E.* ; Atger, F.* ; Weger, M.* ; Gobet, C.* ; Ramnath, D.* ; Charpagne, A.* ; Morin-Rivron, D.* ; Powell, E.E.* ; Sweet, M.J.* ; Masoodi, M.* ; Uhlenhaut, N.H. ; Gachon, F.*

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

Proc. Natl. Acad. Sci. U.S.A. 119:e2200083119 (2022)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
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.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Circadian Clock ; Estrogen ; Growth Hormone ; Insulin Resistance ; Nonalcoholic Fatty Liver Disease
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Journal Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Volume: 119, Issue: 10, Pages: , Article Number: e2200083119 Supplement: ,
Publisher National Academy of Sciences
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Cancer (IDC)