Thyroid Diseases, Metformin and the AMP Kinase Pathway

U. Soyaltin, G. Özgen, T. Kabalak
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Abstract

Introduction Thyroid hormone and adenosine monophosphate-activated protein kinase (AMPK) are 2 major determinants of energy balance. Thyroid hormone is known to be a key factor that stimulates energy use in energy balance. It is involved in almost every stage of energy use. The uptake of energy substances into the cell, their conversion to adenosine triphosphate (ATP) in the mitochondria, and the use of ATP in all cellular processes where energy is required are under the stimulating control of tri-iodothyronine and partially 3,5-diiodo-L-thyronine. A deficiency in thyroid hormone production results in ineffective utilization of energy substrates in the cell, despite their sufficient level. A well-known example of this condiAn increase in the adenosine monophosphate (AMP)/adenosine triphosphate ratio activates AMP-activated protein kinase (AMPK), leading to inhibition of the mammalian target of rapamycin signaling pathway that is associated with autophagy, mitochondriogenesis, glucose uptake, mRNA stabilization, and cell cycle regulation. Metformin activates AMPK and inhibits mitochondrial oxidative phosphorylation. Currently, there is an increasing interest in investigating the effects of metformin on thyroid diseases. Recent data show an association between metformin treatment and lower incidence of thyroid cancer, better survival of patients with thyroid cancer, and lower thyroid volume and nodule size. Insulin-like growth factor receptor and AKT pathways are the AMPK-independent mechanisms through which metformin acts on thyroid diseases. Although metformin has a promising role in adjuvant therapy for thyroid cancers, welldesigned prospective trials are required before reaching a final decision.
甲状腺疾病、二甲双胍和AMP激酶途径
甲状腺激素和腺苷单磷酸活化蛋白激酶(AMPK)是能量平衡的两个主要决定因素。众所周知,甲状腺激素是促进能量平衡中能量使用的关键因素。它几乎涉及能源使用的每个阶段。能量物质进入细胞,在线粒体中转化为三磷酸腺苷(ATP),以及ATP在所有需要能量的细胞过程中的使用都受到三碘甲状腺原氨酸和部分3,5-二碘- l -甲状腺原氨酸的刺激控制。甲状腺激素的缺乏导致细胞内能量底物的无效利用,尽管它们的水平足够。一个众所周知的例子是,单磷酸腺苷(AMP)/三磷酸腺苷比例的增加激活了AMP活化的蛋白激酶(AMPK),从而抑制了雷帕霉素信号通路的哺乳动物靶点,该信号通路与自噬、线粒体形成、葡萄糖摄取、mRNA稳定和细胞周期调节有关。二甲双胍激活AMPK并抑制线粒体氧化磷酸化。目前,人们对二甲双胍对甲状腺疾病的影响越来越感兴趣。最近的数据显示,二甲双胍治疗与较低的甲状腺癌发病率、较好的甲状腺癌患者生存率以及较小的甲状腺体积和结节大小之间存在关联。胰岛素样生长因子受体和AKT通路是二甲双胍作用于甲状腺疾病的不依赖ampk的机制。虽然二甲双胍在甲状腺癌的辅助治疗中有很好的作用,但在做出最终决定之前,需要精心设计的前瞻性试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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