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大脑中的甲状腺激素转运蛋白

Thyroid hormone transporters in the brain.

作者信息

Suzuki Takehiro, Abe Takaaki

机构信息

Division Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan.

出版信息

Cerebellum. 2008;7(1):75-83. doi: 10.1007/s12311-008-0029-9.

Abstract

Thyroid hormone plays an essential role in proper mammalian development of the central nervous system and peripheral tissues. Lack of sufficient thyroid hormone results in abnormal development of virtually all organ systems, a syndrome termed cretinism. In particular, hypothyroidism in the neonatal period causes serious damage to neural cells and leads to mental retardation. Although thyroxine is the major product secreted by the thyroid follicular cells, the action of thyroid hormone is mediated mainly through the deiodination of T(4) to the biologically active form 3,3', 5-triiodo-L-thyronine, followed by the binding of T(3) to a specific nuclear receptor. Before reaching the intracellular targets, thyroid hormone must cross the plasma membrane. Because of the lipophilic nature of thyroid hormone, it was thought that they traversed the plasma membrane by simple diffusion. However, in the past decade, a membrane transport system for thyroid hormone has been postulated to exist in various tissues. Several classes of transporters, organic anion transporter polypeptide (oatp) family, Na(+)/Taurocholate cotransporting polypeptide (ntcp) and amino acid transporters have been reported to transport thyroid hormones. Monocarboxylate transporter8 (MCT8) has recently been identified as an active and specific thyroid hormone transporter. Mutations in MCT8 are associated with severe X-linked psycomotor retardation and strongly elevated serum T3 levels in young male patients. Several other molecules should be contributed to exert the role of thyroid hormone in the central nervous system.

摘要

甲状腺激素在哺乳动物中枢神经系统和外周组织的正常发育中起着至关重要的作用。甲状腺激素缺乏会导致几乎所有器官系统发育异常,即克汀病综合征。特别是新生儿期甲状腺功能减退会对神经细胞造成严重损害并导致智力发育迟缓。虽然甲状腺素是甲状腺滤泡细胞分泌的主要产物,但甲状腺激素的作用主要通过将T4脱碘转化为生物活性形式3,3',5-三碘-L-甲状腺原氨酸,然后T3与特定核受体结合来介导。在到达细胞内靶点之前,甲状腺激素必须穿过质膜。由于甲状腺激素的亲脂性,人们认为它们通过简单扩散穿过质膜。然而,在过去十年中,已推测甲状腺激素在各种组织中存在膜转运系统。据报道,几类转运蛋白,即有机阴离子转运多肽(oatp)家族、Na+/牛磺胆酸盐共转运多肽(ntcp)和氨基酸转运蛋白可转运甲状腺激素。单羧酸转运蛋白8(MCT8)最近被确定为一种活跃且特异性的甲状腺激素转运蛋白。MCT8突变与年轻男性患者严重的X连锁精神运动发育迟缓及血清T3水平显著升高有关。其他几种分子也应有助于甲状腺激素在中枢神经系统中发挥作用。

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