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饮食类型和喂养状态对大鼠肝脏HMG-CoA还原酶调节的影响。

Effect of type of diet and feeding status on modulation of hepatic HMG-CoA reductase in rats.

作者信息

Kelley M J, Story J A

出版信息

Lipids. 1985 Jan;20(1):53-5. doi: 10.1007/BF02534364.

DOI:10.1007/BF02534364
PMID:3968989
Abstract

The effect of diet type and feeding status on hepatic HMG-CoA reductase (HMGR) [mevalonate: NADP+ oxidoreductase (acylating CoA); EC 1.1.1.34] was studied in rats. Animals fed a ground, commercial, stock diet exhibited higher expressed and total activities of HMGR in the fed state than animals fed a semi-purified diet. The differences did not appear in meal-trained animals when measured before the onset of the meal after a 22-hr fast. When expressed activity was taken as a per cent of total activity, fed animals from both diet groups used about 10% of their available activity. When animals on commercial diets were fasted, 20% of the activity was expressed. Fasted animals on the semi-purified diet also increased the per cent of expressed reductase activity, but this increase was not as great (13.3%). These data suggest that, in the rat, regulation of cholesterol synthesis in response to decreased total HMGR during fasting and increased levels after a meal results from alterations in the percentage of enzyme which is expressed. The semi-purified diet used here resulted in consistently lower levels of HMG-CoA reductase activity than the commercial diet regardless of feeding pattern.

摘要

在大鼠中研究了饮食类型和喂养状态对肝脏HMG-CoA还原酶(HMGR)[甲羟戊酸:NADP +氧化还原酶(酰化CoA);EC 1.1.1.34]的影响。喂食磨碎的市售常规饲料的动物在进食状态下的HMGR表达活性和总活性高于喂食半纯化饲料的动物。在禁食22小时后进食开始前测量时,在经进食训练的动物中未出现差异。当以表达活性占总活性的百分比计算时,两个饮食组的进食动物均使用了约10%的可用活性。当喂食商业饲料的动物禁食时,表达的活性为20%。禁食的半纯化饲料喂养的动物也增加了还原酶表达活性的百分比,但增加幅度没有那么大(13.3%)。这些数据表明,在大鼠中,禁食期间总HMGR降低以及进食后水平升高时,胆固醇合成的调节是由于表达的酶百分比发生变化所致。无论喂养方式如何,此处使用的半纯化饲料导致的HMG-CoA还原酶活性水平始终低于商业饲料。

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本文引用的文献

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Reversible modulation of the activities of both liver microsomal hydroxymethylglutaryl coenzyme A reductase and its inactivating enzyme. Evidence for regulation by phosphorylation-dephosphorylation.肝脏微粒体羟甲基戊二酰辅酶A还原酶及其失活酶活性的可逆调节。磷酸化-去磷酸化调节的证据。
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