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肾上腺素和血管紧张素II对正常及遗传性肥胖(ob/ob)小鼠灌注肝脏的分解代谢作用

Catabolic effects of adrenaline and angiotensin II in the perfused liver of normal and genetically obese (ob/ob) mice.

作者信息

Ma G Y, Gove C D, Cawthorne M A, Hems D A

出版信息

Clin Sci (Lond). 1979 May;56(5):493-9. doi: 10.1042/cs0560493.

Abstract
  1. Rapid effects of hormones on the metabolism of glycogen and fatty acids were studied in the perfused liver of normal and genetically obese (ob/ob) mice. 2. In livers from normal and obese mice adrenaline and angiotensin II stimulated glycogenolysis. 3. These hormones inhibited the synthesis de novo of long-chain fatty acids in livers from normal mice, but not in livers from obese mice. 4. The proportion of acetyl-CoA carboxylase in the active form was decreased by adrenaline but not by angiotensin II in livers from obese mice. 5. The potency of hormone effects on liver suggests that they could occur in the intact animal. 6. The results add to the evidence that hepatic fatty acid synthesis in genetically obese (ob/ob) mice is irreversibly resistant to inhibition by a range of hormones. Such resistance could be of primary significance in the pathogenesis of the obesity.
摘要
  1. 在正常和遗传性肥胖(ob/ob)小鼠的灌注肝脏中研究了激素对糖原和脂肪酸代谢的快速作用。2. 在正常和肥胖小鼠的肝脏中,肾上腺素和血管紧张素II刺激糖原分解。3. 这些激素抑制正常小鼠肝脏中长链脂肪酸的从头合成,但不抑制肥胖小鼠肝脏中的合成。4. 在肥胖小鼠的肝脏中,肾上腺素可降低活性形式的乙酰辅酶A羧化酶的比例,但血管紧张素II则不会。5. 激素对肝脏作用的效力表明它们可能在完整动物体内发生。6. 这些结果进一步证明,遗传性肥胖(ob/ob)小鼠的肝脏脂肪酸合成对一系列激素的抑制具有不可逆的抗性。这种抗性可能在肥胖的发病机制中具有重要意义。

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