The stimulation of heart glycolysis by increased workload does not require AMP-activated protein kinase but a wortmannin-sensitive mechanism

被引:38
作者
Beauloye, C
Marsin, AS
Bertrand, L
Vanoverschelde, JL
Rider, MH
Hue, L
机构
[1] UCL, ICP, Hormone & Metab Res Unit, Christian de Duve Inst Cellular Pathol, B-1200 Brussels, Belgium
[2] Univ Louvain, Sch Med, Div Cardiol, Brussels, Belgium
关键词
adenosine monophosphate-activated protein kinase; heart work; fructose-2,6-bisphosphate; protein kinase B; wortmannin;
D O I
10.1016/S0014-5793(02)03552-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Increasing heart workload stimulates glycolysis by enhancing glucose transport and fructose-2,6-bisphosphate (Fru-2,6-P-2), the latter resulting from 6-phosphofructo-2-kinase (PFK-2) activation. Here, we investigated whether adenosine monophosphate (AMP)-activated protein kinase (AMPK) mediates PFK-2 activation in hearts submitted to increased workload. When heart work was increased, PFK-2 activity, Fru-2,6-P-2 content and glycolysis increased, whereas the AMP:adenosine triphosphate (ATP) and phosphocreatine/creatine (PCr:Cr) ratios, and AMPK activity remained unchanged. Wortmannin, the well-known phosphatidylinositol-3-kinase inhibitor, blocked the activation of protein kinase B and the increase in glycolysis and Fru-2,6-P2 content induced by increased work. Therefore, the control of heart glycolysis by contraction differs from that in skeletal muscle where AMPK is involved. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:324 / 328
页数:5
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