ArticleEndocrinology2025
Weight Gain With Advancing Age Is Controlled by the Muscarinic Acetylcholine Receptor M4 in Male Mice.
Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Weight Gain With Advancing Age Is Controlled by the Muscarinic Acetylcholine Receptor M4 in Male Mice.Endocrinology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Obesity is characterized by the excessive accumulation of adipose tissue, and it is a serious global health issue. Understanding the pathology of obesity is crucial for developing effective interventions. In this study, we investigated the role of muscarinic acetylcholine receptor M4 (mAChR-M4) in the regulation of obesity in Chrm4-knockout (M4-KO) mice. Male M4-KO mice showed higher weight gain and accumulation of white adipose tissue (WAT) with advancing age than the wild-type mice. The M4-KO mice also showed increased leptin expression at both the transcription and the translation levels. RNA sequencing and quantitative reverse transcription polymerase chain reaction analyses of subcutaneous adipose tissues revealed that the expression of WAT marker genes was significantly enhanced in the M4-KO mice. In contrast, the expression levels of brown adipose tissue/beige adipose tissue markers were strongly decreased in the M4-KO mice. To identify the Chrm4-expressing cell types, we generated Chrm4-mScarlet reporter mice and examined the localization of the mScarlet fluorescent signals in subcutaneous tissues. Fluorescent signals were prominently detected in WAT and mesenchymal stem cells. Additionally, we also found that choline acetyltransferase was expressed in macrophages, suggesting their involvement in acetylcholine (ACh) secretion. Corroborating this notion, we were able to quantitatively measure the ACh in subcutaneous tissues by liquid chromatography tandem mass spectrometry. Collectively, our findings suggest that endogenous ACh released from macrophages maintains the homeostasis of adipose cell growth and differentiation via mAChR-M4 in male mice. This study provides new insights into the molecular mechanisms underlying obesity and potential targets for therapeutic interventions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.