2024-03-28T12:53:46Z
https://nagoya.repo.nii.ac.jp/oai
oai:nagoya.repo.nii.ac.jp:02005179
2023-03-24T04:18:39Z
1213:1620:1621:1679551797902
AICAR and insulin stimulate glucose uptake in skeletal muscle via nitric oxide independent pathway
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
越中, 敬一
KOSHINAKA, Keiichi
押田, 芳治
OSHIDA, Yoshiharu
韓, 艶清
HAN, Yanqing
佐藤, 祐造
SATO, Yuzo
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.
departmental bulletin paper
名古屋大学総合保健体育科学センター
The Research Center of Health, Physical Fitness and Sports, Nagoya University
2003-03-31
application/pdf
総合保健体育科学
1
26
53
57
Nagoya Journal of Health, Physical Fitness & Sports
0289-5412
https://nagoya.repo.nii.ac.jp/record/2005179/files/njhpfs_26_1_53.pdf
jpn