Role of the alpha2-isoform of AMP-activated protein kinase in the metabolic response of the heart to no-flow ischemia.

作者: Elham Zarrinpashneh , Karla Carjaval , Christophe Beauloye , Audrey Ginion , Philippe Mateo

DOI: 10.1152/AJPHEART.01032.2005

关键词: Protein kinase AAMP-activated protein kinaseGlycogenBiologyCirculatory systemIschemiaGlycolysisEndocrinologyAcetyl-CoA carboxylaseAMPKInternal 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).

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