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大鼠体内胰岛素缺乏对肌肉和肝脏中果糖2,6 -二磷酸水平有不同影响的证据。

Evidence that insulin deficiency in the rat has disparate effects on fructose 2,6-bisphosphate levels in muscle and liver.

作者信息

Dall'Aglio E, Reaven G M, Azhar S

出版信息

Endocrinology. 1986 Jan;118(1):108-11. doi: 10.1210/endo-118-1-108.

DOI:10.1210/endo-118-1-108
PMID:2934240
Abstract

The level of fructose 2,6-bisphosphate (F2,6P2), a potent stimulator of 6-phosphofructo-1-kinase and inhibitor of fructose 1,6-bisphosphatase, was measured in three different muscle types (tensor fascia latae, biceps femoris, and soleus) and in the liver of normal and diabetic rats. The mean (+/- SEM) content of F2,6P2 (nanomoles per g tissue) varied among the three types of skeletal muscle in normal rats, with the biceps femoris having the highest (0.97 +/- 0.15) and the soleus the lowest (0.57 +/- 0.03) levels. However, these differences were unrelated to simultaneous estimates of skeletal muscle activity of 6-phosphofructo-1-kinase activity. The total concentration of F2,6P2 was more than 8-fold higher (8.5 +/- 0.9) in the liver, and this value fell to 5.3 +/- 0.8 (P less than 0.05) after the induction of diabetes with streptozotocin. In contrast, F2,6P2 levels did not fall in skeletal muscle of rats with streptozotocin-induced diabetes, and the concentration actually increased. Thus, the fall in hepatic F2,6P2 concentration associated with insulin deficiency was not observed in skeletal muscle.

摘要

在正常大鼠和糖尿病大鼠的三种不同肌肉类型(阔筋膜张肌、股二头肌和比目鱼肌)以及肝脏中,检测了果糖2,6 - 二磷酸(F2,6P2)的水平。F2,6P2是6 - 磷酸果糖 - 1 - 激酶的强效刺激剂和果糖1,6 - 二磷酸酶的抑制剂。在正常大鼠中,三种骨骼肌类型的F2,6P2平均含量(±标准误,每克组织的纳摩尔数)有所不同,股二头肌的含量最高(0.97±0.15),比目鱼肌的含量最低(0.57±0.03)。然而,这些差异与同时对6 - 磷酸果糖 - 1 - 激酶活性的骨骼肌活性估计无关。肝脏中F2,6P2的总浓度高出8倍多(8.5±0.9),在用链脲佐菌素诱导糖尿病后,该值降至5.3±0.8(P<0.05)。相反,链脲佐菌素诱导的糖尿病大鼠的骨骼肌中F2,6P2水平并未下降,实际上浓度还增加了。因此,在骨骼肌中未观察到与胰岛素缺乏相关的肝脏F2,6P2浓度下降。

相似文献

1
Evidence that insulin deficiency in the rat has disparate effects on fructose 2,6-bisphosphate levels in muscle and liver.大鼠体内胰岛素缺乏对肌肉和肝脏中果糖2,6 -二磷酸水平有不同影响的证据。
Endocrinology. 1986 Jan;118(1):108-11. doi: 10.1210/endo-118-1-108.
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