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反刍动物肝细胞中挥发性脂肪酸的摄取与丙酸代谢

Volatile fatty acid uptake and propionate metabolism in ruminant hepatocytes.

作者信息

Aiello R J, Armentano L E, Bertics S J, Murphy A T

机构信息

Department of Dairy Science, University of Wisconsin, Madison 53706.

出版信息

J Dairy Sci. 1989 Apr;72(4):942-9. doi: 10.3168/jds.S0022-0302(89)79187-6.

Abstract

Previous reports have demonstrated that butyrate inhibits metabolism of propionate by liver cells isolated from sheep and goats. Our objectives were to examine some possible mechanisms for this inhibition and to test for this inhibition in the bovine animal. Incorporation of label from 2.5 mM [2-(14)C]propionate into glucose (nmol propionate/mg cell DM/h) in the presence of 0, 1.25, and 2.5 mM butyrate was 107, 66, and 62 by goat hepatocytes and 79, 25, and 29 by calf hepatocytes; therefore, butyrate inhibited propionate metabolism at least as effectively in calves as in goats. In goat hepatocytes 1.25 mM butyrate reduced 1.25 mM propionate uptake to 46% of control, and 1.25 mM [2-(14)C] propionate incorporation into glucose to 44% of control. Propionate had no effect on butyrate uptake. Isovalerate and valerate tended to be cleared from the media to a greater extent than butyrate but had no effect on propionate uptake. Therefore, inhibition of propionate conversion to glucose by butyrate is specific and is not due to a general competition among VFA for metabolism. Butyrate inhibits hepatic propionate utilization generally, not specifically propionate conversion to glucose. Butyrate also inhibited propionate utilization by goat liver homogenates, indicating that butyrate inhibits propionate metabolism at a step subsequent to propionate transport across the hepatocyte plasma membrane.

摘要

先前的报告表明,丁酸盐可抑制从绵羊和山羊分离出的肝细胞对丙酸盐的代谢。我们的目标是研究这种抑制作用的一些可能机制,并在牛身上测试这种抑制作用。在存在0、1.25和2.5 mM丁酸盐的情况下,山羊肝细胞将2.5 mM [2-(14)C]丙酸盐中的标记掺入葡萄糖(nmol丙酸盐/mg细胞干重/小时)的量分别为107、66和62,小牛肝细胞分别为79、25和29;因此,丁酸盐对丙酸盐代谢的抑制作用在小牛身上至少与在山羊身上一样有效。在山羊肝细胞中,1.25 mM丁酸盐使1.25 mM丙酸盐摄取量降至对照的46%,使1.25 mM [2-(14)C]丙酸盐掺入葡萄糖的量降至对照的44%。丙酸盐对丁酸盐摄取没有影响。异戊酸盐和戊酸盐从培养基中的清除程度往往比丁酸盐更大,但对丙酸盐摄取没有影响。因此,丁酸盐对丙酸盐转化为葡萄糖的抑制作用是特异性的,并非由于挥发性脂肪酸(VFA)之间普遍存在代谢竞争。丁酸盐一般抑制肝脏对丙酸盐的利用,而非特异性地抑制丙酸盐转化为葡萄糖。丁酸盐还抑制山羊肝脏匀浆对丙酸盐的利用,这表明丁酸盐在丙酸盐跨肝细胞质膜转运之后的步骤抑制丙酸盐代谢。

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