| Objective:In recent years,endocrinologists have increasingly emphasized the link between iodine intake and thyroid disease.At present,we believe that the negative feedback of thyroxine on the synthesis and secretion of TSH is mainly mediated by T3.In the pituitary,T3 is mainly due to the local deiodination of T4 via type Ⅱ deiodinase(D2)to T3,and then T3 binds to the thyroid hormone receptor β2 subtype(TRβ2)in the nucleus,thereby regulating TSH.Synthesis and secretion.Although serum concentrations of thyroid hormones are significantly stable,deiodinase can regulate thyroid hormone signaling in a cell-and time-specific manner by controlling the activation and inactivation of thyroid hormones.D2 catalyzes T3 production to enhance thyroid hormone signaling.In contrast,blockade of D2 activity or disruption of the Dio2 gene will result in hypothyroidism.It is noteworthy that D2 is also critical in T4-mediated negative feedback at the hypothalamus level,where T4 inhibits TSH and TRH expression,respectively.This study was to investigate the effect of chronic iodine excess on serum levels of TRH and hypothalamic Ⅱ deiodinases in Wistar rats,and to elucidate the effect of chronic iodine excess on hypothalamic-pituitary-thyroid(HPT)axis hypothalamus levels.The mechanism of thyroid function changes provides a new theoretical explanation for scientific iodine supplementation.Methods:180 4-week-old Wistar rats were randomly divided into 5 groups:normal control group(NI),high-iodine group(3HI)3 times,high-iodine group(6HI)6 times,10 times high iodine group(10HI)and 50-fold high iodine group(50HI).The sodium iodide solution was added to normal diet plus conventional double distilled water,277 ug/L iodine,692 ug/L iodine,1245 ug/L iodine and 6788 ug/L iodine.Rats were sacrificed at 4 weeks,8 weeks,12 weeks and 24 weeks after treatment of factors,respectively.Collect serum from each group.Serum thyroid-stimulating hormone-releasing hormone(TRH)levels were determined by ELISA.Rat brain tissue was collected from each group and used to prepare frozen sections for immunohistochemical detection of D2 protein.Level.Use SPSS 21.0 software to process and analyze the data.Experimental results are expressed as x±SEM.Two or more methods are compared using one-way analysis of variance and two or more methods are compared using the Newman-Keuls test(equal variance)or the Dunnett’s multiple comparison test.The difference is uneven.P<0.05 is a significant difference.Results:1.With the increase of iodine intake and the prolongation of iodine intake time,serum TRH levels in Wistar rats decreased compared with the control group.2.With the increase of iodine intake and the prolongation of iodine intake time,the expression of D2 in Wistar rats increased in each experimental group.Conclusion:The results of this study indicate that excess iodine increases the expression of hypothalamic type Ⅱ deiodinase protein,promotes the conversion of T4 to T3,and enters the pituitary region of paraventricular PVN through the MCT8 transporter and elongate cells.The TRH cell region inhibits the production of TRH and lowers the TRH content in the hypothalamus,which in turn leads to a decrease in the TRH content in the peripheral serum.Although it has been found that type Ⅱ deiodinase activity in pituitary glands is reduced and T4 conversion to T3 is reduced,the inhibitory effect of T3 on TSH is weakened and TSH is elevated,but our experiments show that the elevation of pituitary TSH does not depend on the hypothalamus TRH adjustment.Transport of T3 in elongated cells depends on MCT8 regulation,whereas PPII expressed by extension cells can degrade TRH released in central processes.Therefore,are there other factors that interfere with and influence the reduction of serum TRH that leads to excess iodine?Not clear,pending further study. |
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