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正常及遗传性肥胖-高血糖(ob-ob)小鼠离体灌注肝脏的碳水化合物代谢

Carbohydrate metabolism of the isolated perfused liver of normal and genetically obese--hyperglycaemic (ob-ob) mice.

作者信息

Elliott J, Hems D A, Beloff-Chain A

出版信息

Biochem J. 1971 Dec;125(3):773-80. doi: 10.1042/bj1250773.

Abstract
  1. A technique for perfusion of the mouse liver has been developed, and aspects of carbohydrate metabolism have been investigated in the perfused liver of normal and genetically obese mice, homozygous for the recessive gene ob. 2. Rates of gluconeogenesis in perfused mouse liver were faster than those reported for slices of mouse liver, particularly from lactate and pyruvate. 3. The rate of glycogen breakdown to glucose, but not to lactate, was faster in liver from fed obese mice. 4. The capacity for glycogen synthesis from glucose was enhanced in liver from 20h-starved obese mice. 5. The capacity for gluconeogenesis from a number of substrates was not significantly altered in livers from fed or starved obese mice when compared with that of lean mice. 6. These results suggest that the liver contributes to the hyperglycaemia of the obese mice by increased glycogenolysis, and that liver glycogen in obese mice is maintained by synthesis from dietary glucose.
摘要
  1. 已开发出一种灌注小鼠肝脏的技术,并在正常和因隐性基因ob纯合的遗传性肥胖小鼠的灌注肝脏中研究了碳水化合物代谢的各个方面。2. 灌注小鼠肝脏中的糖异生速率比报道的小鼠肝脏切片的速率要快,尤其是从乳酸和丙酮酸生成糖异生的速率。3. 喂食的肥胖小鼠肝脏中糖原分解为葡萄糖的速率加快,但分解为乳酸的速率未加快。4. 饥饿20小时的肥胖小鼠肝脏中由葡萄糖合成糖原的能力增强。5. 与瘦小鼠相比,喂食或饥饿的肥胖小鼠肝脏中从多种底物进行糖异生的能力没有显著改变。6. 这些结果表明,肝脏通过增加糖原分解导致肥胖小鼠出现高血糖,并且肥胖小鼠的肝脏糖原通过从膳食葡萄糖合成来维持。

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本文引用的文献

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Gluconeogenesis in mouse-liver slices.鼠肝切片中的糖异生作用。
Biochem J. 1966 Dec;101(3):607-17. doi: 10.1042/bj1010607.
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THE CROONIAN LECTURE, 1963. GLUCONEOGENESIS.1963年克罗尼安讲座。糖异生作用
Proc R Soc Lond B Biol Sci. 1964 Mar 17;159:545-64. doi: 10.1098/rspb.1964.0019.

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