The Effects of Iodine Supplementation in Pregnancy on Iodine Status, Thyroglobulin Levels and Thyroid Function Parameters: Results from a Randomized Controlled Clinical Trial in a Mild-to-Moderate Iodine Deficiency Area
Simona CensiSara Watutantrige‐FernandoGiulia GrocciaJacopo MansoMario PlebaniDiego FaggianMonica MionRoberta VenturiniAlessandra AndrisaniA. P. CasaroPietro VitaAlessandra AvogadroMarta CamilotCarla ScaroniLoris BertazzaSusi BarolloCaterina Mian
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Background: Iodine supplementation during pregnancy in areas with mild-to-moderate iodine deficiency is still debated. Methods: A single-center, randomized, single-blind and placebo-controlled (3:2) trial was conducted. We enrolled 90 women before 12 weeks of gestation. From enrollment up until 8 weeks after delivery, 52 women were given an iodine supplement (225 ug/day, potassium iodide tablets) and 38 were given placebo. At recruitment (T0), in the second (T1) and third trimesters (T2), and 8 weeks after delivery (T3), we measured participants’ urinary iodine-to-creatinine ratio (UI/Creat), thyroid function parameters (thyroglobulin (Tg), TSH, FT3, and FT4), and thyroid volume (TV). The newborns’ urinary iodine concentrations were evaluated in 16 cases. Results: Median UI/Creat at recruitment was 53.3 ug/g. UI/Creat was significantly higher in supplemented women at T1 and T2. Tg levels were lower at T1 and T2 in women with UI/Creat ≥ 150 ug/g, and in the Iodine group at T2 (p = 0.02). There was a negative correlation between Tg and UI/Creat throughout the study (p = 0.03, r = −0.1268). A lower TSH level was found in the Iodine group at T3 (p = 0.001). TV increased by +Δ7.43% in the Iodine group, and by +Δ11.17% in the Placebo group. No differences were found between the newborns’ TSH levels on screening the two groups. Conclusion: Tg proved a good parameter for measuring iodine intake in our placebo-controlled series. Iodine supplementation did not prove harmful to pregnancy in areas of mild-to-moderate iodine deficiency, with no appreciable harmful effect on thyroid function.Keywords:
Thyroglobulin
Thyroid-stimulating hormone
Background. Iodine micronutrients are required by the body to generate thyroid hormones. Thyroid hormone deficiency can cause hypothyroidism. Thyroid hormone is produced by the thyroid gland, which the function of the thyroid can be perceived in the levels of TSH and free T4, while iodine status can be appreciated from the iodine content of serum, iodine content of urine and thyroglobulin levels. The aim of this study was to describe the relationship between iodine serum level with thyroid function and iodine status on women of childbearing age with the risk of hypothyroid Method. This was cross sectional study in Purworejo district with a sample of women of childbearing aged 15-45 years with high levels of TSH> 2.5 μIU /mL. The sample size of this study were 88 people. Indicators quantified were the levels of TSH, free T4, iodine serum thyroglobulin levels and urinary iodine concentration (UIE). FreeT4 and TSH and thyroglobulin were measured by ELISA, while iodine serum and UIE were gauged by spectrophotometer method. Results. This study shows the average level of TSH 3.83 μIU / mL±1.5 FreeT4 levels of 1.33 ng / dL 0.25; thyroglobulin levels of 1.20 ng /mL ±0.41; serum iodine content 75.25 μg /L± 41.71 as well as the iodine substance of urine 96.14 μg / L± 65.04. UIE level of was less than 100 μg/L at 64.8%. There was a significant correlation between serum thyroglobulin with the iodine content with a correlation coefficient of 0.352 and p <0.05. Conclusion. For women of childbearing age with the risk of hypothyroidism had a urinary iodine concentration (UIE) less than the normal of 64.8% (problematic IDD) and there was a positive significant correlation between serum levels of iodine with thyroglobulin.
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Thyroid-stimulating hormone
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Background: Iodine supplementation during pregnancy in areas with mild-to-moderate iodine deficiency is still debated. Methods: A single-center, randomized, single-blind and placebo-controlled (3:2) trial was conducted. We enrolled 90 women before 12 weeks of gestation. From enrollment up until 8 weeks after delivery, 52 women were given an iodine supplement (225 ug/day, potassium iodide tablets) and 38 were given placebo. At recruitment (T0), in the second (T1) and third trimesters (T2), and 8 weeks after delivery (T3), we measured participants’ urinary iodine-to-creatinine ratio (UI/Creat), thyroid function parameters (thyroglobulin (Tg), TSH, FT3, and FT4), and thyroid volume (TV). The newborns’ urinary iodine concentrations were evaluated in 16 cases. Results: Median UI/Creat at recruitment was 53.3 ug/g. UI/Creat was significantly higher in supplemented women at T1 and T2. Tg levels were lower at T1 and T2 in women with UI/Creat ≥ 150 ug/g, and in the Iodine group at T2 (p = 0.02). There was a negative correlation between Tg and UI/Creat throughout the study (p = 0.03, r = −0.1268). A lower TSH level was found in the Iodine group at T3 (p = 0.001). TV increased by +Δ7.43% in the Iodine group, and by +Δ11.17% in the Placebo group. No differences were found between the newborns’ TSH levels on screening the two groups. Conclusion: Tg proved a good parameter for measuring iodine intake in our placebo-controlled series. Iodine supplementation did not prove harmful to pregnancy in areas of mild-to-moderate iodine deficiency, with no appreciable harmful effect on thyroid function.
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There is a profound difference in the incidence of thyroid disease between males and females. We have investigated the possibility of a direct effect of sex steroids on the thyroid gland by investigating thyroid function in castrate animals. The rate of thyroid hormone release was estimated by measuring the rate of hydrolysis of labeled thyroglobulin from mouse thyroid glands in vitro. The thyroid glands were labeled in vivo with 131I and then cultured for 20 h in the presence of mononitrotyrosine, an inhibitor of iodotyrosine and deiodinase. The rate of hydrolysis of labeled thyroglobulin was measured as the percentage of radioactivity released as iodotyrosines and iodothyronines into the gland and the medium at the end of incubation. TSH was injected at varying intervals before death in some cases. The basal rates of thyroglobulin hydrolysis were similar in intact and castrate mice, but TSH-stimulated rates were significantly higher in both male and female castrates. Daily treatment of castrates for a week with estradiol or testosterone decreased the rate of thyroglobulin hydrolysis to that seen in intact mice, but dihydrotestosterone was without effect. (Bu)2cAMP added in vitro increased the rate of thyroglobulin hydrolysis in both intact and castrate mice, but the stimulation was significantly greater in the castrates. Basal and TSH-stimulated cAMP levels in the thyroid were similar in castrate and intact mice. There was no difference in thyroidal incorporation of iodine by intact and castrate mice in either presence or absence of TSH. These data suggest the following. 1) Castration results in significantly greater sensitivity to TSH with respect to thyroid hormone secretion. Thyroid hormone synthesis, basal or TSH-stimulated, is, however, unaltered. 2) Estradiol inhibits TSH-stimulated hormone release in castrates. Testosterone has a similar effect, possibly through aromatization to estradiol. 3) The effect of sex hormones is likely to be exerted at a post-cAMP step specific for hormone secretion.
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Recent studies revealed the emerging role of excess uptake of lipids in the development of hypothyroidism. However, the underlying mechanism is largely unknown. We investigated the effect of high-fat diet (HFD) on thyroid function and the role of endoplasmic reticulum (ER) in HFD-induced hypothyroidism. Male Sprague-Dawley rats were fed with HFD or control diet for 18 wk. HFD rats showed an impaired thyroid function, with decreased thyroglobulin (Tg) level. We found the ER stress was triggered in HFD rat thyroid glands and palmitate-treated thyrocytes. Luminal swelling of ER in thyroid epithelial cells of HFD rats was also observed. The rate of Tg degradation increased in palmitate-treated thyrocytes. In addition, applying 4-phenyl butyric acid to alleviate ER stress in HFD rats improved the decrease of Tg and thyroid function. Withdrawal of the HFD improved thyroid function . In conclusion, we demonstrate that ER stress mediates the HFD-induced hypothyroidism, probably by impairing the production of Tg, and attenuation of ER stress improves thyroid function. Our study provides the understanding of how HFD induces hypothyroidism.
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Wistar rats with different levels of iodine nutrition were killed after 3,6 and 12 months of experiments.Serum thyroid hormones were assayed with RIA.The activity of typeⅠdeiodinase(DⅠ)and typeⅡdeiodinase(DⅡ)was measured based on the release of radioiodide from the ~(125)Ⅰ-labeled substrate.The result showed that hypothyroidism reflected by decreased T_4 happened during the initial phase of iodine deficiency.The activity of DⅠand DⅡin rats was raised significantly in iodine deficiency groups.An excess of iodine inhibited DⅠactivity resulting in decreased serum TT_3 and FT_3.However,DⅡactivity increased in rats with iodine excess, attributing to the inactivation of T_3 and T_4 to the substrate of DⅡenzyme.
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Thyroid weight, thyroidal radioiodide uptake, and cyclic AMP-dependent protein kinase activity of a thyroid supernatant fraction were increased significantly in spontaneously hypertensive rats (SHR), apparently because of increased secretion of pituitary TSH. However, the thyroids of SHR did not make supernormal amounts of thyroxine (T4), and thyroidal radioiodine release was apparently impaired. In the SHR, proteolytic enzyme activity was less than normal and the thyroglobulin was more resistant to normal proteolytic enzyme than was control thyroglobulin. Presumably because of these abnormalities, plasma T4 was significantly lower than normal, but triiodothyronine (T3) was normal, as a result of compensatory processes occurring in T3 synthesis and hydrolysis of thyroglobulin. T4 and T3 were less effective in depressing pituitary TSH synthesis and secretion in SHR than in controls, possibly because of an abnormal setting of the “hormostat.” Although the hypothalamic content of TRH was normal in SHR, the exact site of the abnormality in the “hormostat” is not delineated in the present study. (Endocrinology98: 1109, 1976)
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Objective To study the effects of different iodine intake levels on thyroid function at gene expression level in rats. Methods Wistar rats were divided into normal iodine (NI), lower iodine (LI) and higher iodine groups (HI). The urinary iodine excretion, T 4 and T 3 of serum and thyroid tissue were measured, the expressions of thyroglobulin (TG) and thyroid peroxidase (TPO) mRNA in thyroid were determined by RT PCR. Results In LI group, the urinary iodine excretion, T 4, T 3 of serum and thyroid tissue were lower, the expression of TPO mRNA increased markedly, while TG mRNA decreased significantly. In HI group, T 4 showed a decreasing tendency in serum and was markedly reduced in thyroid tissue, along with significantly higher urinary iodine excretion and decreased expressions of TPO mRNA and TG mRNA. Conclusion Lower iodine intake for long term results in severe hypothyroidism, and compensatory increase of TPO mRNA expression but decrease of TG mRNA expression; higher iodine intake inhibits the expressions of both TPO、 TG mRNA as well as thyroid hormone synthesis, which in turn acts as a protective mechanism against iodine excess.
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ABSTRACT It has been suggested that TSH stimulation of the thyroid gland is accompanied by an alteration in the ratio of newly synthesized thyroxine (*T 4 )1)/triiodothyronine (*T 3 ) in favour of *T 3 . Evidence in support of this hypothesis is provided here by the finding that suppression of TSH secretion in rats alters this ratio in the other direction, i. e. in favour of *T 4 . Thus, endogenous TSH stimulation was increased for 4 weeks by iodine deficiency. Its suppression was performed by the administration of T 3 , using a dose of 0.05-0.25 μg/100 g body weight which was injected subcutaneously every 12 hours for three days. The effect of TSH stimulation and suppression could be assessed from the following parameters: thyroid weight and histology, thyroid 131 I uptake, 131 I conversion ratio, hormonal iodine concentration, and TSH level in the plasma. After iodine deficiency the ratio of *T 4 /*T 3 in the thyroid gland changed in favour of *T 3 . This may compensate for the iodine deficiency, since the oxygen consumption and the heart rate of the animals remained in the normal range. After suppression the ratio of *T 4 /*T 3 changed in the opposite direction, i. e. in favour of *T 4 . The extent of the suppression of *T 4 and *T 3 was dependent on the suppression dose used.
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The median urinary iodine concentration (UIC) is a biomarker of iodine intake. According to the World Health Organization, a median UIC in the range 100-199 μg/L indicates adequate and 200-299 μg/L more than adequate intake. Thyroglobulin (Tg) may be a promising functional biomarker of both iodine deficiency and excess.Using a standardized dried blood spots-Tg assay in children, we evaluated the Tg response to both low- and high-iodine intake and estimated the population cutoff point for iodine deficiency or excess. Also, we compared thyroid functions within the UIC ranges of 100-199 vs 200-299 μg/L.We conducted a cross-sectional study in primary schools in 12 countries.SUBJECTS were 6 to 12 years old (n = 2512).We measured UIC, TSH, total T4, Tg, and thyroid antibodies.Over a range of iodine intakes from severely deficient to excessive, Tg concentrations showed a clear U-shaped curve. Compared with iodine-sufficient children, there was a significantly higher prevalence of elevated Tg values in children with iodine deficiency (UIC <100 μg/L) and iodine excess (UIC >300 μg/L). There was no significant change in the prevalence of elevated Tg, TSH, T4, or thyroid antibodies comparing children within the UIC ranges of 100-199 vs 200-299 μg/L.In school-aged children, 1) Tg is a sensitive indicator of both low and excess iodine intake; 2) a median Tg of <13 μg/L and/or <3% of Tg values >40 μg/L indicates iodine sufficiency in the population; 3) the acceptable range of median UIC in monitoring iodized salt programs could be widened to a single category of sufficient iodine intake from 100 to 299 μg/L.
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