给链脲佐菌素诱导的糖尿病大鼠口服钒酸盐可恢复葡萄糖诱导的肝糖原合酶激活。
Oral administration of vanadate to streptozotocin-diabetic rats restores the glucose-induced activation of liver glycogen synthase.
作者信息
Bollen M, Miralpeix M, Ventura F, Toth B, Bartrons R, Stalmans W
机构信息
Afdeling Biochemie, Faculteit Geneeskunde, Katholieke Universiteit Leuven, Belgium.
出版信息
Biochem J. 1990 Apr 1;267(1):269-71. doi: 10.1042/bj2670269.
Abstract
Isolated hepatocytes from streptozotocin-diabetic rats failed to respond to a glucose load with an activation of glycogen synthase. This lesion was associated with severely decreased activities of glycogen-synthase phosphatase and of glucokinase. All these defects were abolished after consumption for 13-18 days of drinking water containing Na3VO4 (0.7 mg/ml), and they were partially restored after 3.5 days, when the blood glucose concentration was already normalized. In all conditions the maximal extent of activation of glycogen synthase in cells closely parallelled the activity of glycogen-synthase phosphatase.
摘要
链脲佐菌素诱导的糖尿病大鼠的分离肝细胞，在葡萄糖负荷刺激下未能激活糖原合酶。这种损伤与糖原合酶磷酸酶和葡萄糖激酶的活性严重降低有关。在饮用含Na3VO4（0.7mg/ml）的水13 - 18天后，所有这些缺陷都消失了，在3.5天后部分得到恢复，此时血糖浓度已恢复正常。在所有情况下，细胞中糖原合酶的最大激活程度与糖原合酶磷酸酶的活性密切平行。
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本文引用的文献
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