| Summary: | 博士 === 中國醫藥大學 === 老化醫學博士學位學程 === 104 === Background
During aging, muscles decline in mass and strength. Loss of muscle function is thought to contribute to the high risk of adverse outcomes such as poor quality of life, falls, and disability. But the risk factors of the loss of skeletal muscle mass remain unclear. This study used the epidemiological and cellular models to explore the effect of inflammation, growth factor and insulin sensitivity on appendicular skeletal muscle mass, and to investigate the effect of advanced glycation end products (AGEs) on myoblast cells.
Methods
In epidemiological study, we recruited the 844 people aged 65 years or older who were registered in the eight administrative neighborhoods (“Li”) of North District, Taichung City, Taiwan, and collected the questionnaire data and blood sample, and measured the body composition, handgrip strength and walking speed from participants. In cellular study, we explored the effect of AGEs on C2C12 cells and investigated the molecular mechanism of AGEs affecting the C2C12 cells.
Results
The serum hs-CRP levels in the obesity only and in the sarcopenic obesity groups were significantly higher than that in the normal group among older male. Appendicular skeletal muscle mass was associated with serum IGF-1 levels among elderly. Variations of the polymorphisms in IGF-1 and IGFBP-3 genes were associated with increased risk of low appendicular skeletal muscle mass. The joint effect of physical inactivity and low level of insulin sensitivity was significantly associated with decreased SMI, gait speed, and grip strength. AGEs suppress C2C12 differentiation via regulation of ERK1/2 and p38 signaling.
Conclusions
Muscle mass is associated with inflammation, growth factor and insulin sensitivity among elderly. Furthermore, AGEs can inhibit the myoblast cells differentiation. From epidemiology to cellular level, insulin and IGF-1 signaling have critical roles in muscle function. These findings may as biomarkers or treatment pathway of sarcopenia.
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