AMPK activation is not critical in the regulation of muscle FA uptake and oxidation during low-intensity muscle contraction
AMPK activation is not critical in the regulation of muscle FA uptake and oxidation during low-intensity muscle contraction
复制标题
DOI：
10.1152/ajpendo.00301.2004
复制
发表时间：
2005-03-01
影响因子：
5.1
通讯作者：
Turcotte, LP
中科院分区：
文献类型：
--
作者：
Raney, MA;Yee, AJ;Turcotte, LP
为了确定amp活化蛋白激酶（AMPK）在调节脂肪酸（FA）摄取和氧化中的作用，我们在休息(R)或电刺激（ES）时向大鼠后肢灌注6 mM葡萄糖、10 muU/ml胰岛素、550 muM棕榈酸酯和[C-14]棕榈酸酯，诱导低强度（0.1 Hz）肌肉收缩，无论是否有2 mM 5-氨基咪唑-4-羧基酰胺-1- β - d -核呋烷苷（AICAR）。AICAR处理显著增加了R期间葡萄糖和FA的摄取（P0.05）。AICAR处理显著提高总FA氧化(P
To determine the role of AMP-activated protein kinase (AMPK) activation on the regulation of fatty acid (FA) uptake and oxidation, we perfused rat hindquarters with 6 mM glucose, 10 muU/ml insulin, 550 muM palmitate, and [C-14] palmitate during rest (R) or electrical stimulation (ES), inducing low-intensity (0.1 Hz) muscle contraction either with or without 2 mM 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). AICAR treatment significantly increased glucose and FA uptake during R (P0.05). AICAR treatment significantly increased total FA oxidation (P