作者: Elham Zarrinpashneh , Karla Carjaval , Christophe Beauloye , Audrey Ginion , Philippe Mateo
DOI: 10.1152/AJPHEART.01032.2005
关键词: Protein kinase A 、 AMP-activated protein kinase 、 Glycogen 、 Biology 、 Circulatory system 、 Ischemia 、 Glycolysis 、 Endocrinology 、 Acetyl-CoA carboxylase 、 AMPK 、 Internal medicine
摘要: AMP-activated protein kinase (AMPK) is a major sensor and regulator of the energetic state cell. Little known about specific role AMPKalpha(2), AMPK isoform in heart, response to global ischemia. We used AMPKalpha(2)-knockout (AMPKalpha(2)(-/-)) mice evaluate consequences AMPKalpha(2) deletion during normoxia ischemia, with glucose as sole substrate. Hemodynamic measurements from echocardiography hearts AMPKalpha(2)(-/-) showed no significant modification compared wild-type animals. In contrast, no-flow ischemia was characterized by more rapid onset ischemia-induced contracture. This ischemic contracture associated decrease ATP content, lactate production, glycogen AMPKbeta(2) content. Hearts were also decreased phosphorylation acetyl-CoA carboxylase Despite an apparent worse metabolic adaptation absence does not exacerbate impairment recovery postischemic contractile function. conclusion, required for heart The remaining AMPKalpha(1) cannot compensate AMPKalpha(2).