@article{oai:nagoya.repo.nii.ac.jp:02005179,
 author = {越中, 敬一 and KOSHINAKA, Keiichi and 押田, 芳治 and OSHIDA, Yoshiharu and 韓, 艶清 and HAN, Yanqing and 佐藤, 祐造 and SATO, Yuzo},
 issue = {1},
 journal = {総合保健体育科学, Nagoya Journal of Health, Physical Fitness & Sports},
 month = {Mar},
 note = {It is well known that muscle contraction, insulin and nitric oxide (NO) increase glucose uptake in skeletal muscle. Some reports suggest that NO is a critical mediator of contraction- and/or insulin- stimulated glucose uptake. The AMP-activated protein kinase (AMPK), a known mediator of contraction-stimulated glucose uptake, is activated by 5-aminoimidazole-4-carboxamicle-1-β-D-ribofuranoside (AICAR) and stimulates glucose uptake. The purpose of the present study was to determine whether NO contributes to AICAR- and/or insulin-stimulated glucose uptake. Isolated epitrochlearis muscles were stimulated by AICAR or insulin with/without wortmannin (100nM), PI-3 kinase inhibitor, or N^G-monomethyl-L-arginine, NO synthase inhibitor (L-NMMA, 300μM), and measured in vitro 2-deoxy-D-[1,2-3H] glucose uptake. AICAR-stimulatd glucose uptake was not inhibited by wortmannin or L-NMMA. Insulin-stimulated glucose uptake was abolished by wortmannin, but L-NMMA did not affect glucose uptake. These results suggest that AICAR and insulin stimulate glucose uptake in skeletal muscle via NO independent pathway.},
 pages = {53--57},
 title = {AICARおよびインスリン刺激による骨格筋グルコース取りこみは一酸化窒素を介さない},
 volume = {26},
 year = {2003}
}