미토콘드리아 생합성과 GLUT4 생합성을 위한 exercise mimetics로서의 PPARδ 효과검정

Abstract

This study aims to analyze the mechanisms of mitochondrial biogenesis and GLUT4 biogenesis by increasing PPARδactivity in skeletal muscle cells and to provide information for the development of exercise mimetics for subjects who have difficulty exercising. To this end, C2C12 skeletal muscle cells were treated with telmisartan, and gene expression related to mitochondrial biogenesis and GLUT4 biogenesis was analyzed. As a result, 10uM telmisartan for six days significantly increased PPARδ expression in skeletal muscle cells. PPARδ increased by telmisartan increased PGC-1α, which plays a key role in mitochondrial biogenesis. Increased expression of PGC-1α increased its downstream signaling, NRF-1 and Tfam, and increased mitochondrial oxidative phosphorylation. In addition, telmisartan increased GLUT4 biogenesis via insulin-independent, but not insulin-dependent, signaling in skeletal muscle cells. Therefore, PPARδwill induce mitochondrial and GLUT4 biosynthesis to treat glucose metabolism and insulin resistance-related diseases during obesity or aging, promote healthy aging, and be very effective as an exercise mimetic agent to improve exercise capacity.