瘦素
自身免疫
甲状腺功能
医学
肥胖
甲状腺
内科学
疾病
作者
Leonidas H. Duntas,Bernadette Biondi
出处
期刊:Thyroid
[Mary Ann Liebert, Inc.]
日期:2012-08-30
卷期号:23 (6): 646-653
被引量:153
标识
DOI:10.1089/thy.2011.0499
摘要
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.
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