Teixeira Patrícia de Fátima Dos Santos, Dos Santos Patrícia Borges, Pazos-Moura Carmen Cabanelas
Endocrine Clinic, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rua Professor Rodolpho Rocco, 255 - Cidade Universitária, Rio de Janeiro, RJ 21941-617, Brazil.
Research Fellow, Medicine School, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Ther Adv Endocrinol Metab. 2020 May 13;11:2042018820917869. doi: 10.1177/2042018820917869. eCollection 2020.
Metabolic syndrome (MetS) and thyroid dysfunction are common in clinical practice. The objectives of this review are to discuss some proposed mechanisms by which thyroid dysfunctions may lead to MetS, to describe the bidirectional relationship between thyroid hormones (THs) and adiposity and finally, to resume a list of recent studies in humans that evaluated possible associations between thyroid hormone status and MetS or its clinical components. Not solely THs, but also its metabolites regulate metabolic rate, influencing adiposity. The mechanisms enrolled are related to its direct effect on adenosine triphosphate (ATP) utilization, uncoupling synthesis of ATP, mitochondrial biogenesis, and its inotropic and chronotropic effects. THs also act controlling core body temperature, appetite, and sympathetic activity. In a bidirectional way, thyroid function is affected by adiposity. Leptin is one of the hallmarks, but the pro-inflammatory cytokines and also insulin resistance impact thyroid function and perhaps its structure. MetS development and weight gain have been positively associated with thyroid-stimulating hormone (TSH) in several studies. Adverse glucose metabolism may be related to hyperthyroidism, but also to reduction of thyroid function or higher serum TSH, as do abnormal serum triglyceride levels. Hypo- and hyperthyroidism have been related to higher blood pressure (BP), that may be consequence of genomic or nongenomic action of THs on the vasculature and in the heart. In summary, the interaction between THs and components of MetS is complex and not fully understood. More longitudinal studies controlling each of all confounding variables that interact with endpoints or exposure factors are still necessary.
代谢综合征(MetS)和甲状腺功能障碍在临床实践中很常见。本综述的目的是讨论甲状腺功能障碍可能导致MetS的一些提出的机制,描述甲状腺激素(THs)与肥胖之间的双向关系,最后总结近期在人类中评估甲状腺激素状态与MetS或其临床组成部分之间可能关联的研究列表。不仅THs,其代谢产物也调节代谢率,影响肥胖。涉及的机制与其对三磷酸腺苷(ATP)利用的直接作用、ATP合成的解偶联、线粒体生物发生及其变力和变时作用有关。THs还通过控制核心体温、食欲和交感神经活动发挥作用。甲状腺功能以双向方式受到肥胖的影响。瘦素是其中一个标志,但促炎细胞因子和胰岛素抵抗也会影响甲状腺功能,甚至可能影响其结构。在多项研究中,MetS的发展和体重增加与促甲状腺激素(TSH)呈正相关。不良的葡萄糖代谢可能与甲状腺功能亢进有关,但也与甲状腺功能减退或血清TSH升高有关,血清甘油三酯水平异常也是如此。甲状腺功能减退和亢进都与高血压(BP)有关,这可能是THs对血管系统和心脏的基因组或非基因组作用的结果。总之,THs与MetS各组成部分之间的相互作用很复杂,尚未完全了解。仍然需要更多的纵向研究来控制与终点或暴露因素相互作用的所有混杂变量。