Inhibition of CILP2 Improves Glucose Metabolism and Mitochondrial Dysfunction in Sarcopenia via the Wnt Signalling Pathway

Autor: Zhibo Deng, Chao Song, Long Chen, Rongsheng Zhang, Linhai Yang, Peng Zhang, Yu Xiu, Yibin Su, Fenqi Luo, Jun Luo, Hanhao Dai, Jie Xu
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Journal of Cachexia, Sarcopenia and Muscle, Vol 15, Iss 6, Pp 2544-2558 (2024)
Druh dokumentu: article
ISSN: 2190-6009
2190-5991
DOI: 10.1002/jcsm.13597
Popis: ABSTRACT Background Skeletal muscle is the primary organ involved in insulin‐mediated glucose metabolism. Elevated levels of CILP2 are a significant indicator of impaired glucose tolerance and are predominantly expressed in skeletal muscle. It remains unclear whether CILP2 contributes to age‐related muscle atrophy through regulating the glucose homeostasis and insulin sensitivity. Methods Initially, the expression levels of CILP2 were assessed in elderly mice and patients with sarcopenia. Lentiviral vectors were used to induce either silencing or overexpression of CILP2 in C2C12 myoblast cells. The effects of CILP2 on proliferation, myogenic differentiation, insulin sensitivity and glucose uptake were evaluated using immunofluorescence, western blotting, real‐time quantitative polymerase chain reaction, RNA sequencing, glucose uptake experiments, dual‐luciferase reporter assays and co‐immunoprecipitation (CO‐IP). An adeno‐associated virus‐9 containing a muscle‐specific promoter was injected into SAMP8 senile mice to observe the efficacy of CILP2 knockout. Results We found that there was more CLIP2 expressed in the skeletal muscle of ageing mice (+1.1‐fold, p
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