饥饿后重新喂食碳水化合物时的肝糖原合成。丙酮酸脱氢酶在肝脏和肝外组织中的调节作用。
Hepatic glycogen synthesis on carbohydrate re-feeding after starvation. A regulatory role for pyruvate dehydrogenase in liver and extrahepatic tissues.
作者信息
Holness M J, French T J, Sugden M C
出版信息
Biochem J. 1986 Apr 15;235(2):441-5. doi: 10.1042/bj2350441.
Abstract
Glucose administration to 48 h-starved rats increased hepatic glucose, lactate, pyruvate and glycogen concentrations and re-activated PDH (pyruvate dehydrogenase complex) in kidney, but not in heart or liver. Dichloroacetate together with glucose re-activated PDH in all three tissues, decreased hepatic lactate and pyruvate concentrations and impaired glycogen resynthesis. Thus on re-feeding, delayed PDH re-activation is important for provision of precursors for hepatic glyconeogenesis.
摘要
给饥饿48小时的大鼠注射葡萄糖后，肝脏中的葡萄糖、乳酸、丙酮酸和糖原浓度升高，肾脏中的丙酮酸脱氢酶复合体（PDH）重新激活，但心脏和肝脏中未出现这种情况。二氯乙酸与葡萄糖一起可使所有三个组织中的PDH重新激活，降低肝脏中的乳酸和丙酮酸浓度，并损害糖原的再合成。因此，在重新喂食时，PDH的延迟重新激活对于为肝脏糖异生提供前体很重要。
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