Maid gene dysfunction promotes hyperobesity via the reduction of adipose tissue inflammation in Mc4r gene-deficient mice

Bibliographic Details
Title: Maid gene dysfunction promotes hyperobesity via the reduction of adipose tissue inflammation in Mc4r gene-deficient mice
Authors: Kyutaro Koyama, Akira Sakamaki, Shinichi Morita, Itsuo Nagayama, Marina Kudo, Yuto Tanaka, Naruhiro Kimura, Yoshihisa Arao, Hiroyuki Abe, Kenya Kamimura, Shuji Terai
Source: Scientific Reports, Vol 14, Iss 1, Pp 1-9 (2024)
Publisher Information: Nature Portfolio, 2024.
Publication Year: 2024
Collection: LCC:Medicine
LCC:Science
Subject Terms: Medicine, Science
More Details: Abstract The onset and progression mechanisms of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are being studied. We developed and analyzed a new mouse model of obesity by combining maternal Id-like molecule (Maid) and melanocortin-4 receptor (Mc4r) gene deletions. Four mice, each at 12 and 28 weeks of age, were analyzed for each genotype: Maid gene knockout, Mc4r gene knockout, combined Mc4r and Maid gene knockout, and Mc4r gene knockout with a high-fat diet. Mice with a combined deficiency of Mc4r and Maid gene showed significantly more severe obesity compared to all other genotypes, but no liver fibrosis or a decline in metabolic status were observed. In visceral white adipose tissue, Maid and Mc4r gene knockout mice had fewer CD11c-positive cells and lower mRNA expression of both inflammatory and anti-inflammatory cytokines. Furthermore, Maid and Mc4r gene knockout mice showed lower expression of adipocytokines in visceral white adipose tissue and uncoupling protein-1 in scapular brown adipose tissue. The expression of adipocytokines and uncoupling protein-1 is regulated by sympathetic nerve signaling that contribute severe obesity in Maid and Mc4r gene knockout mice. These mechanisms contribute hyperobesity in Maid and Mc4r gene knockout mice.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2045-2322
Relation: https://doaj.org/toc/2045-2322
DOI: 10.1038/s41598-024-72217-1
Access URL: https://doaj.org/article/0bde0df3e10b4ad49ffb6c6165fcbe67
Accession Number: edsdoj.0bde0df3e10b4ad49ffb6c6165fcbe67
Database: Directory of Open Access Journals
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More Details
ISSN:20452322
DOI:10.1038/s41598-024-72217-1
Published in:Scientific Reports
Language:English