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肥胖、甲状腺功能与自身免疫之间的相互关系:瘦素的多重作用。

The interconnections between obesity, thyroid function, and autoimmunity: the multifold role of leptin.

机构信息

Endocrine Unit, Evgenidion Hospital, University of Athens, Medical School, 115 28 Athens, Greece.

出版信息

Thyroid. 2013 Jun;23(6):646-53. doi: 10.1089/thy.2011.0499. Epub 2013 Apr 4.

Abstract

BACKGROUND

There is increasing evidence that changes in thyroid function are associated with obesity, a condition associated with a chronic low-grade state of inflammation. Meanwhile, recent data have disclosed a relation between obesity and thyroid autoimmunity, with the adipocyte hormone leptin appearing to be the key factor linking these two conditions.

SUMMARY

Leptin has variably been implicated in thyroid function, while recent findings suggest that leptin resistance may mitigate leptin deficiency and enhance autoimmunity in obese subjects via mechanisms operating independently of thyroid function. The development of resistance to the weight-lowering effects of leptin in obesity might well be initiated by activation of inflammatory signaling, which substantially contributes to the derangement of immune response and propagation of autoimmunity in susceptible individuals.

CONCLUSIONS

Regulation of inflammasome-derived cytokines in obesity is an important step in controlling the trigger of thyroid autoimmunity. The clarification of the pathways may offer innovative therapeutic targets in obesity and thyroid autoimmunity.

摘要

背景

越来越多的证据表明,甲状腺功能的变化与肥胖有关,而肥胖是一种与慢性低度炎症状态相关的疾病。与此同时,最近的数据揭示了肥胖与甲状腺自身免疫之间的关系,脂肪细胞激素瘦素似乎是将这两种情况联系起来的关键因素。

概述

瘦素对甲状腺功能的影响各不相同,而最近的研究结果表明,瘦素抵抗可能通过独立于甲状腺功能的机制减轻肥胖患者的瘦素缺乏并增强自身免疫。肥胖患者对瘦素降低体重作用的抵抗可能是由炎症信号的激活引发的,这在很大程度上导致了免疫反应的紊乱和自身免疫的传播。

结论

肥胖症中炎性小体衍生细胞因子的调节是控制甲状腺自身免疫触发因素的重要步骤。阐明这些途径可能为肥胖症和甲状腺自身免疫提供创新的治疗靶点。

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