ArticleJournal of the Chinese Medical Association : JCMA2026
Cholecystokinin inhibits myotube fusion and may contribute to sarcopenia: Evidence from clinical and C2C12 myoblast studies.
Article in Journal of the Chinese Medical Association : JCMA, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSarcopenia, characterized by a progressive loss of muscle mass and strength, is increasingly recognized in aging populations. Although gut hormones may play a role in sarcopenia pathogenesis, their clinical relevance remains unclear. In this study, we investigated whether circulating cholecystokinin (CCK) is associated with sarcopenia and its effects on myogenesis.
methodsFrom 2018 to 2022, 179 adults (aged ≥65 years) at the Taipei Veterans General Hospital were enrolled and classified as having sarcopenia or not based on the 2019 Asian Working Group for Sarcopenia criteria. Comprehensive geriatric assessments, including Mini-Nutritional Assessment Short-Form (MNA-SF), Instrumental Activities of Daily Living (IADL), and bioelectrical impedance analysis were performed. Circulating levels of CCK, ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY were measured from blood samples collected at enrollment. In the experimental arm, murine C2C12 myoblasts were cultured and exposed to different concentrations of CCK. Myogenic differentiation was assessed by western blotting of MYH1/2 expression, and myotube fusion was quantified using immunofluorescence-derived fusion indices.
resultsThe enrolled participants comprised 84 non-sarcopenic and 95 sarcopenic subjects. Compared with the non-sarcopenic group, sarcopenic individuals had significantly higher serum levels of CCK and GLP-1, lower MNA-SF scores, Barthel Index, IADL scores, and higher frailty prevalence. In multivariate logistic regression analysis, age, BMI, and MNA-SF remained significant independent predictors of sarcopenia. However, after adjustment, CCK was not independently associated with sarcopenia. In vitro, CCK had no significant effects on early myoblast differentiation, although it significantly inhibited myotube fusion, indicating specific disruption of a key step in muscle development.
conclusionAlthough CCK was not independently associated with sarcopenia after adjustment, elevated serum CCK and its inhibitory effects on myotube fusion indicate a potential pathophysiological role in muscle degeneration.
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