A novel compound heterozygous leptin receptor mutation causes more severe obesity than in Lepr


Journal

Journal of lipid research
ISSN: 1539-7262
Titre abrégé: J Lipid Res
Pays: United States
ID NLM: 0376606

Informations de publication

Date de publication:
2021
Historique:
received: 08 03 2021
revised: 03 08 2021
accepted: 04 08 2021
pubmed: 15 8 2021
medline: 25 3 2022
entrez: 14 8 2021
Statut: ppublish

Résumé

The leptin receptor (Lepr) pathway is important for food intake regulation, energy expenditure, and body weight. Mutations in leptin and the Lepr have been shown to cause early-onset severe obesity in mice and humans. In studies with C57BL/6NCrl mice, we found a mouse with extreme obesity. To identify a putative spontaneous new form of monogenic obesity, we performed backcross studies with this mouse followed by a quantitative trait locus (QTL) analysis and sequencing of the selected chromosomal QTL region. We thereby identified a novel Lepr mutation (C57BL/6N-Lepr

Identifiants

pubmed: 34390703
pii: S0022-2275(21)00087-0
doi: 10.1016/j.jlr.2021.100105
pmc: PMC8450258
pii:
doi:

Substances chimiques

Receptors, Leptin 0
leptin receptor, mouse 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

100105

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article.

Auteurs

Claudia Berger (C)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany.

Henrike O Heyne (HO)

Medical Department, Institute for Human Genetics, University of Leipzig Medical Center, Leipzig, Germany; Institute for Molecular Medicine Finland: FIMM, Helsinki, Finland; Broad Institute of Harvard and MIT, Cambridge, MA, USA.

Tina Heiland (T)

Medical Department, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig Medical Center, Leipzig, Germany.

Sebastian Dommel (S)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany.

Corinna Höfling (C)

Medical Department, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig Medical Center, Leipzig, Germany.

Esther Guiu-Jurado (E)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany.

Jana Lorenz (J)

Medical Department, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig Medical Center, Leipzig, Germany.

Steffen Roßner (S)

Paul-Flechsig-Institute for Brain Research, University of Leipzig, Leipzig, Germany.

Michael Dannemann (M)

Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany; Institute of Genomics, University of Tartu, Tartu, Estonia.

Janet Kelso (J)

Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany.

Peter Kovacs (P)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany.

Matthias Blüher (M)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany; Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig, Leipzig, Germany.

Nora Klöting (N)

Medical Department III, Endocrinology, Nephrology, Rheumatology, CRC1052, University of Leipzig Medical Center, Leipzig, Germany; Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig, Leipzig, Germany. Electronic address: nora.kloeting@helmholtz-muenchen.de.

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Classifications MeSH