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      Association between serum TSH levels and metabolic components in euthyroid subjects: a nationwide population-based study

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          Abstract

          Background

          Whether a relationship exists between various metabolic factors and thyroid-stimulating hormone (TSH) levels in euthyroid persons remains unknown. This study aims to explore the relationship between TSH levels and metabolic factors in euthyroid individuals.

          Methods

          A total of 2,663 subjects were enrolled from a nationwide population-based cross-sectional survey of iodine nutrition, thyroid disease and diabetes in China (2014–2017). Euthyroid individuals were divided into four groups according to quartiles of TSH levels: group A (n=305, 0.3–1.3 mIU/L), group B (n=829, 1.3–2.2 mIU/L), group C (n=673, 2.2–3.2 mIU/L) and group D (n=349, 3.2–4.2 mIU/L). Anthropometric parameters, biochemical indicators and TSH levels were determined.

          Results

          A total of 2,156 euthyroid subjects with serum TSH levels within the normal range accounted for 86.8% of the sample. The systolic blood pressure (SBP) in group D was significantly higher than that in the other three groups. Group C displayed significantly lower thyroid peroxidase antibody (TPOAb) levels than the other three groups. Group C also had lower anti-thyroglobulin antibody (TgAb) levels than groups A and D, whereas the TgAb levels in group B were only lower than those in group A. Spearman’s or Pearson’s linear regression analysis showed that SBP (r=0.054; P=0.013) was positively correlated with TSH, but cholesterol (TC) (r=−0.043, P=0.047) was negatively correlated with TSH. Multiple stepwise regression analysis revealed that SBP, the urinary iodine concentration (UIC), waist circumference (WC), body mass index (BMI), TC, triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-C) were independent predictors of serum TSH levels.

          Conclusion

          This large population-based study demonstrates a significant interaction between metabolic factors and TSH levels. An adverse weight status, high blood pressure levels, blood lipid metabolism disorder and excessive iodine intake may be early manifestations of thyroid disease in euthyroid subjects.

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          Most cited references31

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          Effect of iodine intake on thyroid diseases in China.

          Iodine is an essential component of thyroid hormones; either low or high intake may lead to thyroid disease. We observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake: mildly deficient (median urinary iodine excretion, 84 microg per liter), more than adequate (median, 243 microg per liter), and excessive (median, 651 microg per liter). Participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, we examined the effect of regional differences in iodine intake on the incidence of thyroid disease. Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the cumulative incidence of overt hypothyroidism was 0.2 percent, 0.5 percent, and 0.3 percent, respectively; that of subclinical hypothyroidism, 0.2 percent, 2.6 percent, and 2.9 percent, respectively; and that of autoimmune thyroiditis, 0.2 percent, 1.0 percent, and 1.3 percent, respectively. Among subjects with euthyroidism and antithyroid antibodies at baseline, the five-year incidence of elevated serum thyrotropin levels was greater among those with more than adequate or excessive iodine intake than among those with mildly deficient iodine intake. A baseline serum thyrotropin level of 1.0 to 1.9 mIU per liter was associated with the lowest subsequent incidence of abnormal thyroid function. More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis. Copyright 2006 Massachusetts Medical Society.
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            Metabolic Syndrome Among Adults in China: The 2010 China Noncommunicable Disease Surveillance.

            In China, data on the prevalence of metabolic syndrome have been rare recently.
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              Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions.

              TRH is a tripeptide amide that functions as a neurotransmitter but also serves as a neurohormone that has a critical role in the central regulation of the hypothalamic-pituitary-thyroid axis. Hypophysiotropic TRH neurons involved in this neuroendocrine process are located in the hypothalamic paraventricular nucleus and secrete TRH into the pericapillary space of the external zone of the median eminence for conveyance to anterior pituitary thyrotrophs. Under basal conditions, the activity of hypophysiotropic TRH neurons is regulated by the negative feedback effects of thyroid hormone to ensure stable, circulating, thyroid hormone concentrations, a mechanism that involves complex interactions between hypophysiotropic TRH neurons and the vascular system, cerebrospinal fluid, and specialized glial cells called tanycytes. Hypophysiotropic TRH neurons also integrate other humoral and neuronal inputs that can alter the setpoint for negative feedback regulation by thyroid hormone. This mechanism facilitates adaptation of the organism to changing environmental conditions, including the shortage of food and a cold environment. The thyroid axis is also affected by other adverse conditions such as infection, but the central mechanisms mediating suppression of hypophysiotropic TRH may be pathophysiological. In this review, we discuss current knowledge about the mechanisms that contribute to the regulation of hypophysiotropic TRH neurons under physiological and pathophysiological conditions.
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                Author and article information

                Journal
                Diabetes Metab Syndr Obes
                Diabetes Metab Syndr Obes
                DMSO
                dmso
                Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Dove
                1178-7007
                22 August 2019
                2019
                : 12
                : 1563-1569
                Affiliations
                [1 ]Department of Endocrinology and Nephrology, Chongqing University Central Hospital, Chongqing Emergency Medical Center , Chongqing, People’s Republic of China
                [2 ]Department of Endocrinology, Southwest Hospital, Army Medical University , Chongqing, People’s Republic of China
                [3 ]Department of Endocrinology, General Hospital of Xinjiang Military Region, PLA , Urumqi, People’s Republic of China
                [4 ]Department of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University , Chongqing, People’s Republic of China
                Author notes
                Correspondence: Wuquan DengDepartment of Endocrinology and Nephrology, Chongqing University Central Hospital, Chongqing Emergency Medical Center , No. 1 Jiankang Road, Yuzhong District, Chongqing, People’s Republic of ChinaTel +86 236 369 2185Email wuquandeng@gmail.com
                Article
                202769
                10.2147/DMSO.S202769
                6709806
                31686877
                ea6328a9-ef1c-4ec7-a843-0eaa6fb9f673
                © 2019 Ren et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 24 January 2019
                : 30 July 2019
                Page count
                Figures: 2, Tables: 2, References: 32, Pages: 7
                Categories
                Original Research

                Endocrinology & Diabetes
                thyroid-stimulating hormone,metabolic syndrome,iodine nutrition,euthyroid state

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