甲状腺激素对胰岛β细胞的影响及其可能机制  

Influence of thyroid hormone on islet 15 cell and its possible mechanisms

作　　者：李莉华[1] 樊继援[1] 

机构地区：[1]天津医科大学总医院内分泌科,300052

出　　处：《国际内分泌代谢杂志》2008年第2期129-131,142,共4页International Journal of Endocrinology and Metabolism

摘　　要：甲状腺功能亢进（甲亢）患者可并发糖耐量减低甚至糖尿病，其机制可能是甲状腺激素（TH）毒性诱发的胰岛β细胞分泌功能损害。TH可通过核受体、促甲状腺激素释放激素（TRH）以及生长抑素、儿茶酚胺、连接肽酶和细胞因子途径等影响胰岛β细胞功能。由于甲亢状态下存在明显的氧化应激，而氧化应激可导致胰岛β细胞凋亡，诱发2型糖尿病，推测TH也可能通过氧化应激机制造成胰岛β细胞凋亡和胰岛素分泌缺陷。Hyperthyroidism is often combined with impaired glucose tolerance （IGT）or diabetes. The mechanism may be the impairment of the secretary function of β cells induced by thyrotoxicosis. Thyroid hormone （TH） can influence the β-cells by different pathways such as binding to nuclear receptor, by TRH, somatostatin,catecholamine as well as connecting peptidase and cytokine. There exists prominent oxidative stress at thyrotoxicosis and it is documented that oxidative stress can induce apoptosis of β cells and lead to type 2 diabetes（T2DM）. It is presumed that oxidative stress provoked by TH could induce apoptosis of β- cells and influence its secretary function, so IGT/T2DM occurs subsequently.

关 键 词：甲状腺功能亢进 糖尿病 甲状腺激素 核受体 胰岛Β细胞 氧化应激 

分 类 号：R587.1[医药卫生—内分泌] R581[医药卫生—内科学]