Glycogen metabolism in the liver of the foetal rat.
Glycogen metabolism in the liver of the foetal rat.
复制标题
胎鼠肝脏中的糖原代谢。
作者：
P. Devos;H. Hers
1.通过在妊娠19.5天时向母体注射微量[6-（3）H]葡萄糖，标记大鼠胎仔肝脏中存在的糖原。标记物给药后4 h掺入糖原中的放射性在38 h后仍存在。这种放射性的大部分在多糖的外链上。这些结果表明，胎仔肝脏中通常几乎没有糖原降解。相反，母亲被麻醉的胎儿肝脏中的糖原分解非常迅速。2.糖原合成酶在妊娠第16天存在于肝脏中，浓度高达成人的30%，但基本上是一种无活性（B）酶。在第18天和第19天之间合成酶磷酸酶的出现对应于合成酶a的出现和糖原合成的开始。从第19天到第21.5天，胎儿肝脏中存在的合成酶a的量刚好足以说明糖原沉积的实际速率。3.胎肝中总磷酸化酶的含量从第16天到出生时持续增加。然而，不可能精确测量非麻醉胎儿肝脏中酶的a和B形式。以糖原分解率作为磷酸化酶活性的适当指标，我们得出结论，在正常条件下，这种酶在胎肝中几乎完全处于非活性形式。4.因此，妊娠晚期肝内糖原的积累可以用合成速率相对较慢和几乎完全没有降解来解释。
1. The glycogen present in the liver of rat foetuses was labelled by injecting a trace amount of [6-(3)H]glucose into the mother at 19.5 days of gestation. The radioactivity incorporated in the glycogen 4h after the administration of the label was still present 38h later. A large proportion of this radioactivity was on the outer chains of the polysaccharide. These results indicate that there is normally almost no glycogen degradation in the foetal liver. In contrast, glycogen breakdown occurs very rapidly in the livers of foetuses whose mother is anaesthetized. 2. Glycogen synthetase is present in the liver at day 16 of gestation at a concentration as high as 30% of that in the adult, but essentially as an inactive (b) enzyme. The appearance of synthetase phosphatase between days 18 and 19 corresponds to that of synthetase a and to the beginning of glycogen synthesis. From day 19 to 21.5 the amount of synthetase a present in the foetal liver is just sufficient to account for the actual rate of glycogen deposition. 3. The content of total phosphorylase in the foetal liver increases continuously from day 16 to birth. However, a precise measurement of the a and b forms of the enzyme in the liver of non-anaesthetized foetuses is not possible. Taking the rate of glycogenolysis as an appropriate index of phosphorylase activity, we conclude that this enzyme is almost entirely in the inactive form in the foetal liver under normal conditions. 4. The accumulation of glycogen in the liver during late pregnancy may therefore be explained by a relatively slow rate of synthesis and a nearly total absence of degradation.