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

Zhibo Deng, Chao Song, Long Chen, Rongsheng Zhang, Linhai Yang, Peng Zhang, Yu Xiu, Yibin Su, Fenqi Luo, Jun Luo, Hanhao Dai, Jie Xu

Shengli Clinical Medical College, Fujian Medical University, Fuzhou, People's Republic of China. · pubmed

Paper

Abstract

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.

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Research summary

The paper investigates the role of CILP2 in glucose metabolism and mitochondrial dysfunction in the context of sarcopenia, which is an age-related condition. By exploring the potential mechanisms through which CILP2 affects insulin sensitivity and glucose homeostasis, the research addresses a factor that may contribute to age-related muscle atrophy. However, while the findings may contribute to understanding sarcopenia, the impact appears to be limited and more incremental rather than groundbreaking in the broader context of longevity research.

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