Academic Journal
Maid gene dysfunction promotes hyperobesity via the reduction of adipose tissue inflammation in Mc4r gene-deficient mice
Title: | Maid gene dysfunction promotes hyperobesity via the reduction of adipose tissue inflammation in Mc4r gene-deficient mice |
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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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ISSN: | 20452322 |
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DOI: | 10.1038/s41598-024-72217-1 |
Published in: | Scientific Reports |
Language: | English |