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Hepatic mitochondrial inner-membrane properties beta-oxidation and carnitine palmitoyltransferases A and B. Effects of genetic obesity and starvation.

机译:肝线粒体内膜特性β氧化和肉碱棕榈酰转移酶A和B。遗传性肥胖和饥饿的影响。

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摘要

Hepatic mitochondrial carnitine palmitoyltransferase (CPT) properties, beta-oxidation of palmitoyl-CoA and membrane polarization were measured in lean and obese Zucker rats. The Vmax. of the 'outer' carnitine palmitoyltransferase ('CPT-A') increased with starvation, with no change in the Km for either carnitine or palmitoyl-CoA. The Ki for malonyl-CoA increased with starvation in lean rats, but not in obese rats. The Vmax. of the 'inner' enzyme ('CPT-B'), as measured by using inverted submitochondrial vesicles, increased with starvation in obese rats only, with no change in the Km for either carnitine or palmitoyl-CoA. The Ki for malonyl-CoA was 2-5-fold higher in inverted vesicles than in intact mitochondria, and showed no alteration with starvation. The activities of both enzymes correlated positively with each other and with beta-oxidation, and inversely with membrane polarization. Malonyl-CoA had little effect on gross membrane fluidity in the Zucker rat, as reflected by diphenylhexatriene fluorescence polarization. The results indicate that both enzymes are related and respond similarly to alterations in membrane fluidity. Membrane fluidity may provide a mechanism for co-ordinated control of CPT activity on both sides of the mitochondrial inner membrane.
机译:在瘦和肥胖的Zucker大鼠中测量了肝线粒体肉碱棕榈酰转移酶(CPT)的性质,棕榈酰CoA的β-氧化和膜极化。 Vmax。饥饿时,“外部”肉碱棕榈酰转移酶(“ CPT-A”)的增加,而肉碱或棕榈酰-CoA的Km不变。饥饿大鼠中丙二酰辅酶A的Ki随饥饿而增加,但肥胖大鼠中Ki随饥饿而增加。 Vmax。通过使用倒置的线粒体小泡测量的“内部”酶(“ CPT-B”)的含量仅在肥胖大鼠中随饥饿而增加,而肉碱或棕榈酰-CoA的Km不变。丙二酰辅酶A的Ki在倒囊中比在完整的线粒体中高2-5倍,并且没有饥饿引起的改变。两种酶的活性相互之间呈正相关,与β氧化呈正相关,与膜极化呈负相关。如二苯基己三烯荧光偏振所反映的那样,丙二酰辅酶A对Zucker大鼠的总膜流动性影响很小。结果表明,两种酶都相关,并且对膜流动性的变化具有相似的响应。膜的流动性可能为协调控制线粒体内膜两侧的CPT活性提供了一种机制。

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