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外文期刊>The biochemical journal
>Inactivation of pyruvate dehydrogenase complex in heart muscle mitochondria of gold-thioglucose-induced obese mice is not due to a stable increase in activity of pyruvate dehydrogenase kinase
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Inactivation of pyruvate dehydrogenase complex in heart muscle mitochondria of gold-thioglucose-induced obese mice is not due to a stable increase in activity of pyruvate dehydrogenase kinase
pThe proportion of pyruvate dehydrogenase (PDH) complex in the active dephosphorylated form was decreased (compared with fed lean control mice) in heart muscle mitochondria after the induction of obesity with gold-thioglucose (by 54%) or starvation of lean mice for 48 h (by 81%). The effects of obesity to inactivate PDH complex were demonstrable 4 weeks after administration of gold-thioglucose, and occurred despite significant hyperinsulinaemia in obese animals. Phosphorylation and inactivation of PDH complex in mouse heart muscle in starvation was attributed to a stable increase (2.7-fold) in the activity of PDH kinase as measured in extracts of mitochondria mediated by increased specific activity of a protein activator of PDH kinase (KAP) [Denyer, Kerbey & Randle (1986) Biochem. J. 239, 347-354]. In obese mice no such increase in kinase activity was observed, and we conclude that phosphorylation and inactivation of PDH complex in heart muscle in obesity is not mediated by KAP, but rather is a consequence of increased lipid oxidation./p
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机译:>在金-硫代葡萄糖诱导肥胖(或肥胖小鼠)饥饿后,心肌线粒体中活性脱磷酸化形式的丙酮酸脱氢酶(PDH)复合物的比例降低(与进食的瘦对照小鼠相比)持续48小时(减少81%)。肥胖使PDH复合物失活的影响在给予金-硫葡萄糖后4周已证实,尽管肥胖动物中存在大量高胰岛素血症,但仍会发生肥胖。饥饿时小鼠心肌中PDH复合物的磷酸化和失活归因于PDH激酶活性的稳定增加(2.7倍),这是由PDH激酶(KAP)的蛋白活化剂增加的比活性介导的线粒体提取物中测得的[Denyer,Kerbey& Randle(1986)生物化学。 J. 239,347-354]。在肥胖小鼠中,未观察到激酶活性的这种增加,并且我们得出结论,肥胖者心肌中PDH复合物的磷酸化和失活不是由KAP介导的,而是脂质氧化增加的结果。 p>
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