Investigations of thyroid hormones and antibodies in obesity: Leptin levels are associated with thyroid autoimmunity independent of bioanthropometric, hormonal, and weight-related determinants

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Abstract

Objectives: Obesity can alter the thyroid hormone status as a result of a dysregulated endocrine loop between the hypothalamo-pituitary unit and adipose tissue. The adipocytokine leptin has been shown to promote autoimmunity; hence, we aimed to clarify whether leptin excess of obesity could increase the susceptibility to develop autoimmune thyroid disease (AITD). Study design: This cross-sectional study was performed in a tertiary care center. Methods: Free thyroid hormones, TSH, thyroglobulin, and antithyroid antibodies levels were tested in 165 obese and 118 lean subjects. Results were plotted against variables related to body composition, leptin levels, glucose homeostasis, energy expenditure, and pattern of weight accrual. Results: Compared with controls, obese patients had lower free T3 levels and free T 4 levels (P < 0.01), greater prevalence of hypothyroidism (P < 0.05), and higher commonness of antithyroid antibodies (P < 0.05). As a marker of AITD, thyroid peroxidase antibodies were more frequent in the obese group (P < 0.01). Correlation analysis showed that leptin levels were associated with AITD (P < 0.01) independent of bioanthropometric variables. Multiple logistic regression analysis in pooled groups identified female sex and leptin as significant predictors of AITD. Conclusions: Obesity increases the susceptibility to harbor AITD with an emerging role for leptin as a peripheral determinant, which needs to be confirmed in future investigations. Copyright © 2010 by The Endocrine Society.

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Marzullo, P., Minocci, A., Tagliaferri, M. A., Guzzaloni, G., Di Blasio, A., De Medici, C., … Liuzzi, A. (2010). Investigations of thyroid hormones and antibodies in obesity: Leptin levels are associated with thyroid autoimmunity independent of bioanthropometric, hormonal, and weight-related determinants. Journal of Clinical Endocrinology and Metabolism, 95(8), 3965–3972. https://doi.org/10.1210/jc.2009-2798

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