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4至5月龄的喂食及禁食状态下的遗传性肥胖小鼠肝脏葡萄糖利用的酶活性

Enzyme activities of hepatic glucose utilization in the fed and fasting genetically obese mouse at 4-5 months of age.

作者信息

Hron W T, Sobocinski K A, Menahan L A

出版信息

Horm Metab Res. 1984 Dec;16 Suppl 1:32-6. doi: 10.1055/s-2007-1014893.

Abstract

Activities of key enzymes in hepatic glucose utilization were compared between obese (C57BL/6J ob/ob) mice, their lean controls and outbred Swiss albino mice in the fed condition and during fasting. As liver hyperplasia and hepatocyte hypertrophy were present in the ob/ob mice at 4-5 months of age and changes in hepatic cellularity did occur with fasting, enzyme activity was expressed on the basis of protein, DNA, and wet weight. In the fed state, activities of glucokinase + hexokinase (glucose phosphorylating capability), phosphofructokinase and pyruvate kinase were significantly greater in livers of ob/ob mice when compared to those of the lean control. Glucokinase + hexokinase activities in livers of ob/ob mice remained significantly higher throughout the 48 h fast yet the activities of hepatic phosphofructokinase and pyruvate kinase, when expressed per g wet wt or mg protein, decreased so that a statistical difference from the fasted lean control was no longer detected. When expressed per 100 g body weight, hepatic glucokinase + hexokinase as well as phosphofructokinase and pyruvate kinase activities in obese mice were higher both in the fed and fasted states when compared to lean controls in the comparable nutritional condition. This increased capacity of key enzyme activities in hepatic glucose utilization can be attributed to liver hyperplasia found in ob/ob mice in both the fed and fasted condition. While higher hepatic glucose phosphorylating capability was maintained during fasting, the elevated specific activities of hepatic phosphofructokinase and pyruvate kinase in the obese mouse in the fed state decreased with starvation to values found in the lean control.

摘要

在喂食状态和禁食期间,比较了肥胖(C57BL/6J ob/ob)小鼠、其瘦对照以及远交系瑞士白化小鼠肝脏中葡萄糖利用关键酶的活性。由于4 - 5月龄的ob/ob小鼠存在肝脏增生和肝细胞肥大,且禁食时肝细胞数量确实发生了变化,所以酶活性以蛋白质、DNA和湿重为基础来表示。在喂食状态下,与瘦对照相比,ob/ob小鼠肝脏中葡萄糖激酶 + 己糖激酶(葡萄糖磷酸化能力)、磷酸果糖激酶和丙酮酸激酶的活性显著更高。在48小时禁食期间,ob/ob小鼠肝脏中的葡萄糖激酶 + 己糖激酶活性一直显著更高,但以每克湿重或毫克蛋白质表示时,肝脏磷酸果糖激酶和丙酮酸激酶的活性降低,以至于与禁食的瘦对照不再有统计学差异。当以每100克体重表示时,与处于相同营养状态的瘦对照相比,肥胖小鼠在喂食和禁食状态下肝脏中的葡萄糖激酶 + 己糖激酶以及磷酸果糖激酶和丙酮酸激酶活性均更高。肝脏葡萄糖利用关键酶活性的这种增加能力可归因于在喂食和禁食状态下ob/ob小鼠中发现的肝脏增生。虽然禁食期间肝脏葡萄糖磷酸化能力保持较高,但肥胖小鼠在喂食状态下肝脏磷酸果糖激酶和丙酮酸激酶升高的比活性随着饥饿而降低至瘦对照中的水平。

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