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食物剥夺对非泌乳奶牛酮血症、酮生成及肝脏中间代谢的影响。

Effects of food deprivation on ketonaemia, ketogenesis and hepatic intermediary metabolism in the non-lactating dairy cow.

作者信息

Baird G D, Heitzman R J, Reid I M, Symonds H W, Lomax M A

出版信息

Biochem J. 1979 Jan 15;178(1):35-44. doi: 10.1042/bj1780035.

Abstract
  1. The aim of this work was to investigate why non-lactating dairy cows are less susceptible to the development of ketonaemia during food deprivation than are dairy cows in early lactation. 2. The first experiment (Expt. A) consisted of determining the effect of 6 days of food deprivation on the concentrations of ketone bodies, and of metabolites related to the regulation of ketogenesis, in jugular blood and liver of non-lactating cows. 3. During the food deprivation, blood ketone-body concentrations rose significantly, but to a value that was only 16% of that achieved in lactating cows deprived of food for 6 days [Baird, Heitzman & Hibbitt (1972) Biochem. J. 128, 1311--1318]. 4. In the liver, food deprivation caused: a rise in ketone-body concentrations; a fall in the concentration of glycogen and of various intermediates of the Embden-Meyerhof pathway and the tricarboxylic acid cycle; an increase in cytoplasmic reduction; a decrease in the [total NAD+]/[total NADH] ratio; a decrease in energy charge. These changes were all qualitatively similar to those previously observed in the livers of the food-deprived lactating cows. 5. There appeared therefore to be a discrepancy in the food-deprived non-lactating cows between the absence of marked ketonaemia and the occurrence of metabolic changes within the liver suggesting increased hepatic ketogenesis. This discrepancy was partially resolved in Expt. B by the observation in two catheterized non-lactating cows that, although there was a 2-fold increase in hepatic ketogenesis during 6 days of food deprivation, ketogenesis from the splanchnic bed as a whole (i.e. gut and liver combined) declined slightly owing to cessation of gut ketogenesis.
摘要
  1. 本研究的目的是探究为何非泌乳期奶牛在食物匮乏期间比泌乳早期的奶牛更不易发生酮血症。2. 第一个实验(实验A)包括测定6天食物匮乏对非泌乳期奶牛颈静脉血和肝脏中酮体浓度以及与酮体生成调节相关的代谢物浓度的影响。3. 在食物匮乏期间,血酮体浓度显著升高,但仅达到饥饿6天的泌乳奶牛所达到值的16%[贝尔德、海茨曼和希比特(1972年)《生物化学杂志》128卷,1311 - 1318页]。4. 在肝脏中,食物匮乏导致:酮体浓度升高;糖原以及糖酵解途径和三羧酸循环的各种中间产物浓度降低;细胞质还原增加;[总NAD⁺]/[总NADH]比值降低;能量电荷减少。这些变化在性质上均与先前在饥饿的泌乳奶牛肝脏中观察到的变化相似。5. 因此,在饥饿的非泌乳期奶牛中,明显不存在显著酮血症与肝脏内发生的表明肝酮生成增加的代谢变化之间似乎存在差异。在实验B中,通过对两只插有导管的非泌乳期奶牛的观察部分解决了这一差异,即尽管在6天食物匮乏期间肝酮生成增加了2倍,但由于肠道酮生成停止,整个内脏床(即肠道和肝脏结合)的酮生成略有下降。

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本文引用的文献

1
Biochemical aspects of bovine ketosis.牛酮病的生化方面。
Biochem J. 1968 May;107(5):683-9. doi: 10.1042/bj1070683.

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