The insulin-like effects of tungstate (W) and molybdate (Mo) were studied in rat adipocytes and compared to those of vanadate. Other than being less potent, W and Mo resembled vanadate in stimulating lipogenesis, in activating glucose oxidation, in enhancing rate of hexose uptake, and in inhibiting lipolysis. Tungstate and molybdate did not activate the insulinreceptor tyrosine kinase (InsRTK). Quercetin which blocks InsRTK activity and insulin stimulation of glucose metabolism, failed to inhibit when these bioeffects were stimulated by W or Mo. The metalooxide, however, activated a staurosporine sensitive non receptor, cytosolic protein tyrosine kinase (CytPTK), and staurosporine blocked W or Mo dependent lipogenesis in rat adipocytes. Staurosporine did not prevent Mo and W either from activating hexose transport, or from inhibiting lipolysis. Tungstate and molybdate were less effective than vanadate in inhibiting adipose PTPases in cell free systems. Membranal PTPases were more sensitive to W and Mo inhibition than cytosolic PTPases. While the presence of a nucleophile such as hydroxylamine reversed inhibition of PTPase by vanadate it did not affect inhibition by W or Mo. In summary, the insulinomimetic effects of W and Mo appear to resemble qualitatively that of vanadate in all respects. Both act in an insulin receptor-independent-fashion, activate CytPTK and trigger additional effects that are not mediated by the InsRTK or by CytPTK. The quantitative differences may be attributed to reduced capacity of W and Mo relative to vanadate to inhibit the relevant PTPases in intact cells.

译文

在大鼠脂肪细胞中研究了钨酸盐 (W) 和钼酸盐 (Mo) 的胰岛素样作用,并与钒酸盐进行了比较。除了效力较弱之外,W和Mo在刺激脂肪生成,激活葡萄糖氧化,提高己糖摄取率和抑制脂解作用方面类似于钒酸盐。钨酸盐和钼酸盐不会激活胰岛素受体酪氨酸激酶 (InsRTK)。槲皮素可阻断InsRTK活性和胰岛素刺激葡萄糖代谢,但当W或Mo刺激这些生物效应时,槲皮素无法抑制。然而,金属氧化物激活了星形孢菌素敏感的非受体,胞质蛋白酪氨酸激酶 (cyptk),星形孢菌素阻断了大鼠脂肪细胞中W或Mo依赖性脂肪生成。星形孢菌素不能阻止Mo和W激活己糖转运或抑制脂解。钨酸盐和钼酸盐在抑制无细胞系统中的脂肪PTPases的效果不如钒酸盐。膜al PTPases对W和Mo抑制比胞质PTPases更敏感。虽然亲核试剂 (例如羟胺) 的存在使钒酸盐对PTPase的抑制作用逆转,但不会影响W或Mo的抑制作用。总而言之,W和Mo的胰岛素模拟作用在所有方面都与钒酸盐的定性相似。两者均以不依赖胰岛素受体的方式起作用,激活cyptk并触发InsRTK或cyptk未介导的其他作用。定量差异可能归因于W和Mo相对于钒酸盐抑制完整细胞中相关PTPases的能力降低。

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