Beta-adrenergic modulation of insulin binding in skeletal muscle.
Beta-adrenergic modulation of insulin binding in skeletal muscle.
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骨骼肌中胰岛素结合的β-肾上腺素能调节。
DOI：
10.1152/ajpendo.1986.250.2.e198
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Koerker,DJ
中科院分区：
文献类型：
--
作者：
Webster,B;Vigna,SR;Paquette,T;Koerker,DJ
先前已证明高生理浓度 (13.1 nM) 的肾上腺素 (E) 和急性运动 (AEx) 均可增加骨骼肌中 125 I-胰岛素的结合。为了研究肾上腺素对结合的影响位点和机制以及肾上腺素和 AEx 增强的胰岛素结合之间可能存在的联系，我们测量了三种不同制剂中的胰岛素结合：1) 来自比目鱼肌的粗膜，在体外与 13.1 nM E 一起孵育，2) 结合测定中存在 E 的粗膜，以及 3) 存在 E 的纯化质膜。在低浓度的胰岛素下，肾上腺素在所有三种制剂中的结合分别增强了 169%、144% 和 164%，但在高浓度下几乎没有影响。因此，肾上腺素似乎对质膜有作用。普萘洛尔 (10 µM) 是一种 β-肾上腺素能拮抗剂，可阻断 E 增强的胰岛素结合，当添加到 AEx 大鼠的比目鱼肌和趾长伸肌制成的粗膜中时，可逆转运动时观察到的结合增加。这表明E-增强的胰岛素结合是由β-肾上腺素能受体介导的，并且AEx通过β-肾上腺素能受体增强胰岛素结合。原钒酸钠 (3 mM) 是一种磷酸酪氨酰蛋白磷酸酶抑制剂，也能抑制 E 导致的胰岛素结合增加，这意味着 E 可能通过激活磷酸酪氨酰蛋白磷酸酶来增加胰岛素结合，从而降低质膜蛋白（可能是胰岛素受体）的磷酸化。
Both a high physiological concentration (13.1 nM) of epinephrine (E) and acute exercise (AEx) have previously been shown to increase 125I-insulin binding in skeletal muscle. To investigate the site and mechanism of the effect of epinephrine on binding and the possible link between epinephrine- and AEx-enhanced insulin binding, we measured insulin binding in three different preparations: 1) crude membranes derived from whole soleus muscle incubated in vitro with 13.1 nM E, 2) crude membranes with E present in the binding assay, and 3) purified plasma membranes with E present. Epinephrine enhanced binding in all three preparations by 169, 144, and 164%, respectively, at low concentrations of insulin but had little effect at high concentrations. Epinephrine, therefore appears to have its effect at the plasma membrane. Propranolol (10 microM), a beta-adrenergic antagonist, blocked E-enhanced insulin binding and when added to crude membranes made from soleus and extensor digitorum longus muscle of AEx rats reversed the increase in binding seen with exercise. This indicates that E-enhanced insulin binding is mediated by beta-adrenergic receptors and that AEx enhances insulin binding via beta-adrenergic receptors. Sodium orthovanadate (3 mM), a phosphotyrosyl-protein phosphatase inhibitor, also inhibited the increase in insulin binding due to E, implying that E may increase insulin binding by activating a phosphotyrosyl-protein phosphatase which decreases the phosphorylation of a plasma membrane protein, presumably the insulin receptor.