id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-012771-3ukffdmq	Xu, Deng-qiu	The hypoglycemic mechanism of catalpol involves increased AMPK-mediated mitochondrial biogenesis	2020-01-14		.txt	text/plain	4686	283	43	Catalpol increased mitochondrial biogenesis, evidenced by significant elevations in the number of mitochondria, mitochondrial DNA levels, and the expression of three genes associated with mitochondrial biogenesis: peroxisome proliferator-activated receptor gammaco-activator 1 (PGC-1α), mitochondrial transcription factor A (TFAM) and nuclear respiratory factor 1 (NRF1). The expression levels of three genes associated with mitochondrial biogenesis (PGC-1α, NRF1, and TFAM) were markedly decreased in the skeletal muscle of db/db mice, but these decreases were reversed by catalpol (Fig. 1i) , as revealed by Western blotting (Fig. 1j, k) . Using db/db mice and C2C12 cells, we showed that catalpol increases mitochondrial biogenesis by activating the AMPK/PGC-1α/TFAM signaling pathway, which improves both mitochondrial function and glucose homeostasis in skeletal muscle (Fig. 6) . Catalpol increased AMPK/PGC-1α/TFAM-mediated mitochondrial biogenesis in skeletal muscle cells. The catalpol-induced activation of AMPK/PGC-1α/TFAM signaling increased mitochondrial biogenesis in skeletal muscle, thereby increasing glucose uptake and ATP production.	./cache/cord-012771-3ukffdmq.txt	./txt/cord-012771-3ukffdmq.txt