肝脏磷酸化酶激酶缺乏大鼠的血糖稳态
Blood glucose homeostasis in rats with a deficiency of liver phosphorylase kinase.
作者信息
Conaglen J C, Williams A B, Malthus R S, Glover D, Sneyd J G
出版信息
Am J Physiol. 1985 Jan;248(1 Pt 1):E44-50. doi: 10.1152/ajpendo.1985.248.1.E44.
The glycogen storage disorder (gsd/gsd) rat has little or no phosphorylase kinase activity in the liver and is unable to break down liver glycogen on fasting. Nevertheless, gsd/gsd rats do not become hypoglycaemic on fasting. Gsd/gsd rats showed a decreased rate of glucose turnover measured with [6-3H]glucose. Perfused livers from gsd/gsd rats showed decreased rates of gluconeogenesis from lactate and alanine when the results were expressed per gram of liver, but the total glucose produced per liver was normal. Measurement of gluconeogenesis in vivo using [14C]-bicarbonate showed that gsd/gsd rats had a decreased rate of glucose production from substrates that enter the gluconeogenic pathway before pyruvate. We conclude that gsd/gsd rats have adapted to unavailability of liver glycogen by decreasing peripheral uptake of glucose and not by increasing gluconeogenesis.
糖原贮积病（gsd/gsd）大鼠肝脏中磷酸化酶激酶活性很低或几乎没有，禁食时无法分解肝糖原。然而，gsd/gsd大鼠禁食时不会出现低血糖。用[6-³H]葡萄糖测定，gsd/gsd大鼠的葡萄糖周转率降低。当结果以每克肝脏表示时，gsd/gsd大鼠的灌注肝脏中乳酸和丙氨酸的糖异生率降低，但每个肝脏产生的总葡萄糖量正常。使用[¹⁴C] - 碳酸氢盐在体内测量糖异生表明，gsd/gsd大鼠从丙酮酸之前进入糖异生途径的底物产生葡萄糖的速率降低。我们得出结论，gsd/gsd大鼠通过降低外周葡萄糖摄取而非增加糖异生来适应肝糖原的缺乏。
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