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甲状腺自身调节:碘对培养的甲状腺细胞中葡萄糖转运的影响。

Thyroid autoregulation: effect of iodine on glucose transport in cultured thyroid cells.

作者信息

Filetti S, Vetri M, Damante G, Belfiore A

出版信息

Endocrinology. 1986 Apr;118(4):1395-400. doi: 10.1210/endo-118-4-1395.

DOI:10.1210/endo-118-4-1395
PMID:3948787
Abstract

The nonmetabolizable glucose analogs, [3H]2-deoxy-D-glucose and [3H]O-methyl-D-glucose, were used to determine whether iodide influences glucose transport in porcine cells in primary culture. Incubation with iodide (3 h) decreased basal glucose transport with a half-maximum at NaI 3 X 10(-5) M and maximum at 10(-4) M. Iodide (10(-6) M to 10(-4) M) also abolished the stimulatory effect of TSH (1 mU/ml) on glucose transport. The iodide effect on [3H]2-deoxy-D-glucose transport had the following characteristics: 1) it was abolished 24 h after incubation in iodide-free medium; 2) it was prevented by methimazole (3 mM), and correlated with newly formed organic iodine, 3) and it affected the maximum velocity (Vmax) of glucose transport, reducing it from 25.1 to 14.4 and 12.0 nmol/(min mg protein) at 10(-5) M and 10(-4) M NaI, without affecting the Michaelis-Menten constant (Km) (6mM). Iodide-treated cells had a reduced specific binding of [3H]cytochalasin B (38% and 47% with respect to control cells at 10(-5) M and 10(-4) M NaI). These data suggest that iodide treatment reduces the functional carriers mediating glucose transport in the thyroid.

摘要

使用不可代谢的葡萄糖类似物[3H]2-脱氧-D-葡萄糖和[3H]O-甲基-D-葡萄糖来确定碘化物是否影响原代培养的猪细胞中的葡萄糖转运。用碘化物孵育(3小时)可降低基础葡萄糖转运,在碘化钠浓度为3×10(-5)M时达到半数最大效应,在10(-4)M时达到最大效应。碘化物(10(-6)M至10(-4)M)也消除了促甲状腺激素(1 mU/ml)对葡萄糖转运的刺激作用。碘化物对[3H]2-脱氧-D-葡萄糖转运的影响具有以下特点:1)在无碘化物培养基中孵育24小时后这种影响消失;2)甲巯咪唑(3 mM)可阻止这种影响,且与新形成的有机碘相关;3)它影响葡萄糖转运的最大速度(Vmax),在10(-5)M和10(-4)M碘化钠时,Vmax从25.1降至14.4和12.0 nmol/(分钟·毫克蛋白质),而不影响米氏常数(Km)(6 mM)。经碘化物处理的细胞对[3H]细胞松弛素B的特异性结合减少(在10(-5)M和10(-4)M碘化钠时,相对于对照细胞分别减少38%和47%)。这些数据表明,碘化物处理减少了甲状腺中介导葡萄糖转运的功能性载体。

相似文献

1
Thyroid autoregulation: effect of iodine on glucose transport in cultured thyroid cells.甲状腺自身调节:碘对培养的甲状腺细胞中葡萄糖转运的影响。
Endocrinology. 1986 Apr;118(4):1395-400. doi: 10.1210/endo-118-4-1395.
2
Thyrotropin stimulates glucose transport in cultured rat thyroid cells.促甲状腺激素刺激培养的大鼠甲状腺细胞中的葡萄糖转运。
Endocrinology. 1987 Jun;120(6):2576-81. doi: 10.1210/endo-120-6-2576.
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Autoregulation by iodine of thyroid protein synthesis: influence of iodine on amino acid transport in cultured thyroid cells.
Endocrinology. 1984 Apr;114(4):1379-85. doi: 10.1210/endo-114-4-1379.
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Effects of thyrotropin, carbachol, and protein kinase-C stimulators on glucose transport and glucose oxidation by primary cultures of dog thyroid cells.促甲状腺激素、卡巴胆碱和蛋白激酶-C刺激剂对犬甲状腺细胞原代培养物葡萄糖转运和葡萄糖氧化的影响。
Endocrinology. 1988 Sep;123(3):1288-95. doi: 10.1210/endo-123-3-1288.
5
Human erythrocyte sugar transport is incompatible with available carrier models.人类红细胞的糖转运与现有的载体模型不相符。
Biochemistry. 1996 Aug 13;35(32):10411-21. doi: 10.1021/bi953077m.
6
Cultured thyroid cell adenosine 3',5'-cyclic monophosphate response to thyrotropin: loss and restoration of sensitivity to iodide inhibition.培养的甲状腺细胞对促甲状腺素的3',5'-环磷酸腺苷反应:对碘抑制敏感性的丧失与恢复
Endocrinology. 1977 Mar;100(3):755-64. doi: 10.1210/endo-100-3-755.
7
Effects of iodide on thyroid follicle structure and electrophysiological potentials of cultured thyroid cells.碘化物对甲状腺滤泡结构及培养甲状腺细胞电生理电位的影响。
Endocrinology. 1985 Jul;117(1):71-6. doi: 10.1210/endo-117-1-71.
8
On the mechanism of inhibition by iodine of the thyroid adenylate cyclase response to thyrotropic hormone.关于碘对甲状腺腺苷酸环化酶促甲状腺激素反应的抑制机制。
Endocrinology. 1976 Jul;99(1):11-22. doi: 10.1210/endo-99-1-11.
9
The actions of iodide and TSH on thyroid cells showing a dual control system for the iodide pump.
Endocrinology. 1974 May;94(5):1465-74. doi: 10.1210/endo-94-5-1465.
10
A growth stimulatory effect of iodide is suggested by its effects on c-myc messenger ribonucleic acid levels, [3H]thymidine incorporation, and mitotic activity of porcine follicle cells in suspension culture.碘化物对悬浮培养的猪卵泡细胞的c-myc信使核糖核酸水平、[3H]胸腺嘧啶核苷掺入及有丝分裂活性的影响表明,碘化物具有生长刺激作用。
Endocrinology. 1987 Aug;121(2):757-64. doi: 10.1210/endo-121-2-757.

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