PuSH - Publication Server of Helmholtz Zentrum München: A novel compound heterozygous leptin receptor mutation causes more severe obesity than in Lepr<em><sup>db/db</sup></em> mice.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Berger, C.* ; Heyne, H.O.* ; Heiland, T.* ; Dommel, S.* ; Höfling, C.* ; Guiu-Jurado, E.* ; Roßner, S.* ; Dannemann, M.* ; Kelso, J.* ; Kovacs, P.* ; Blüher, M. ; Klöting, N.

A novel compound heterozygous leptin receptor mutation causes more severe obesity than in Lepr^db/db mice.

J. Lipid Res. 62:100105 (2021)

Publ. Version/Full Text

DOI

PMC

	Open Access Gold

Abstract
Metrics
Extra information

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^{L536Hfs∗6-1NKB}), which is located at chromosome 4, exon 11 within the CRH2-leptin binding site. Compared to C57BL/6N mice, Lepr^L536Hfs∗6 develop early onset obesity and their body weight exceeds that of Lepr^db/db mice at an age of 30 weeks. Similar to Lepr^db/db mice, the Lepr^L536Hfs∗6 model is characterized by hyperphagia, obesity, lower energy expenditure and activity, hyperglycemia, and hyperinsulinemia compared to C57BL/6N mice. Crossing Lepr^db/wt with Lepr^{L536Hfs∗6/wt} mice results in compound heterozygous Lepr^{L536Hfs∗6/db} mice, which develop even higher body weight and fat mass than both homozygous Lepr^db/db and Lepr^L536Hfs∗6 mice. Our study suggests that the phenotype of monogenic Lepr deficient mice depends on the molecular localization of the Lepr mutation. Compound heterozygous Lepr deficiency affecting functionally different regions of the Lepr causes more severe obesity than the parental homozygous mutations.

Impact Factor

Scopus SNIP

Altmetric

5.922

0.000

PuSH - Publication Server of Helmholtz Zentrum München

A novel compound heterozygous leptin receptor mutation causes more severe obesity than in Leprdb/db mice.

A novel compound heterozygous leptin receptor mutation causes more severe obesity than in Lepr^db/db mice.