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体内甲状腺功能亢进和减退大鼠的葡萄糖代谢。用14C和3H标记的葡萄糖获得的葡萄糖周转率值和无效循环活性。

Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Glucose-turnover values and futile-cycle activities obtained with 14C- and 3H-labelled glucose.

作者信息

Okajima F, Ui M

出版信息

Biochem J. 1979 Aug 15;182(2):565-75. doi: 10.1042/bj1820565.

Abstract
  1. A trace amount of glucose labelled with 14C uniformly and with 3H at position 2, 3 or 6 was injected intravenously into starved rats to measure the turnover rate of blood glucose. 2. Reliable estimates were made based on the semilogarithmic plot of specific radioactivity of the glucose contained in whole blood samples taken from the tail vein. 3. Glucose turned over more rapidly in hyperthyroid and more slowly in hypothyroid than in euthyroid rats. The percentage contribution of glucose recycling (determined from the difference in replacement rates between [U-14C]glucose and [6-3H]glucose) to the glucose utilization increased on induction of hyperthyroidism. 4. Futile cycles between glucose and glucose 6-phosphate (determined from the difference between replacement rates of [2-3H]glucose and [6-3H]glucose) were activated and inactivated by induction of hyperthyroid and hypothyroid states respectively. 5. The hepatic content of glycogen was much lower in hyper- and hypo-thyroid than in euthyroid rats. The enhanced glucose production in hyperthyroid rats resulted from not only activationof hepatic gluconeogenesis but also diversion of the final product of gluconeogenesis from liver glycogen to blood glucose. In hypothyroidism, the inhibition of gluconeogensis led to suppression of both glucose production and glycogenesis in the liver.
摘要
  1. 将微量均匀标记有(^{14}C)且在第2、3或6位标记有(^{3}H)的葡萄糖静脉注射到饥饿的大鼠体内,以测量血糖的周转率。2. 根据从尾静脉采集的全血样本中葡萄糖比放射性的半对数图进行可靠估计。3. 与甲状腺功能正常的大鼠相比,甲状腺功能亢进的大鼠葡萄糖周转更快,甲状腺功能减退的大鼠葡萄糖周转更慢。甲状腺功能亢进时,葡萄糖再循环(由[U-(^{14}C)]葡萄糖和[6-(^{3}H)]葡萄糖的替代率差异确定)对葡萄糖利用的贡献百分比增加。4. 葡萄糖与6-磷酸葡萄糖之间的无效循环(由[2-(^{3}H)]葡萄糖和[6-(^{3}H)]葡萄糖的替代率差异确定)分别因甲状腺功能亢进和减退状态的诱导而被激活和失活。5. 甲状腺功能亢进和减退的大鼠肝脏糖原含量远低于甲状腺功能正常的大鼠。甲状腺功能亢进大鼠葡萄糖生成增加不仅是由于肝脏糖异生的激活,还由于糖异生的终产物从肝糖原转向血糖。在甲状腺功能减退时,糖异生的抑制导致肝脏葡萄糖生成和糖原合成均受到抑制。

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