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去神经支配骨骼肌中的胰岛素作用。糖原合成刺激减少不涉及胰岛素结合减少的证据。

Insulin action in denervated skeletal muscle. Evidence that the reduced stimulation of glycogen synthesis does not involve decreased insulin binding.

作者信息

Smith R L, Lawrence J C

出版信息

J Biol Chem. 1985 Jan 10;260(1):273-8.

PMID:3917433
Abstract

The motor nerves to rat soleus and epitrochlearis muscles were sectioned 1-3 days before the muscles were incubated in vitro to assess insulin action and binding. The hormonal stimulation of [U-14C]glucose into glycogen in both muscles was decreased by over 80% after 3 days of denervation. Associated with the reductions in glycogen synthesis were losses in the ability of insulin to activate glycogen synthase. Even so, denervated and control muscles bound the same amounts of 125I-labeled insulin over a wide range of insulin concentrations. Scatchard analysis indicates that denervation changed neither receptor numbers nor affinities. The results presented strongly suggest that the loss of the ability of insulin to stimulate glycogen synthesis following denervation is the result of a postreceptor defect.

摘要

在对大鼠比目鱼肌和肱三头肌进行体外培养以评估胰岛素作用和结合情况的1 - 3天前,切断其运动神经。去神经支配3天后,两种肌肉中[U - 14C]葡萄糖转化为糖原的激素刺激作用降低了80%以上。与糖原合成减少相关的是胰岛素激活糖原合酶能力的丧失。即便如此,在广泛的胰岛素浓度范围内,去神经支配的肌肉和对照肌肉结合的125I标记胰岛素量相同。Scatchard分析表明,去神经支配既未改变受体数量,也未改变亲和力。所呈现的结果有力地表明,去神经支配后胰岛素刺激糖原合成能力的丧失是受体后缺陷的结果。

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