Hepatic FTO is dispensable for the regulation of metabolism but counteracts HCC development in vivo.


Journal

Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730

Informations de publication

Date de publication:
12 2020
Historique:
received: 18 04 2020
revised: 15 09 2020
accepted: 16 09 2020
pubmed: 22 9 2020
medline: 8 9 2021
entrez: 21 9 2020
Statut: ppublish

Résumé

Single-nucleotide polymorphisms in the FTO gene encoding an m We generated mice with hepatic FTO deficiency (FTO In long-term DEN experiments, FTO Collectively, our study demonstrates that hepatic FTO is dispensable for the control of energy homeostasis and glucose metabolism. However, we show a protective function of FTO in liver carcinogenesis and suggest the FTO-dependent dynamic mRNA demethylation of Cul4a in the initiation of HCC development contributes to this effect.

Identifiants

pubmed: 32956847
pii: S2212-8778(20)30159-9
doi: 10.1016/j.molmet.2020.101085
pmc: PMC7560164
pii:
doi:

Substances chimiques

FTO protein, mouse EC 1.14.11.-
Alpha-Ketoglutarate-Dependent Dioxygenase FTO EC 1.14.11.33
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

101085

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK020541
Pays : United States

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier GmbH.. All rights reserved.

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Auteurs

Melanie J Mittenbühler (MJ)

Max Planck Institute for Metabolism Research, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Cologne, 50931, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Germany.

Katarzyna Saedler (K)

Max Planck Institute for Metabolism Research, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Cologne, 50931, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Germany.

Hendrik Nolte (H)

Max Planck Institute for Biology of Ageing, Cologne, 50931, Germany.

Lara Kern (L)

Max Planck Institute for Metabolism Research, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Cologne, 50931, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Germany.

Jun Zhou (J)

Division of Nutritional Sciences, Cornell University, Ithaca, NY, 14853, USA.

Shu-Bing Qian (SB)

Division of Nutritional Sciences, Cornell University, Ithaca, NY, 14853, USA.

Lydia Meder (L)

Department I of Internal Medicine, University Hospital Cologne, Cologne, 50931, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany.

Roland T Ullrich (RT)

Department I of Internal Medicine, University Hospital Cologne, Cologne, 50931, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany; Center for Integrated Oncology Cologne/Bonn, University Hospital Cologne, 50931, Cologne, Germany; University Hospital Bonn, Bonn, 53172, Germany.

Jens C Brüning (JC)

Max Planck Institute for Metabolism Research, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Cologne, 50931, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany. Electronic address: thomas.wunderlich@sf.mpg.de.

F Thomas Wunderlich (FT)

Max Planck Institute for Metabolism Research, Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Cologne, 50931, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, 50931, Germany. Electronic address: bruening@sf.mpg.de.

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