The Role of Thyroid Hormone Synthesis Gene-Related miRNAs Profiling in Structural and Functional Changes of The Thyroid Gland Induced by Excess Iodine.

At recent years, the impairment caused by iodine excess are paid more attention. However, there is still largely unknown about the exact mechanism induced by excessive iodine. MiRNAs have been found to act as biomarkers for a variety of diseases, whereas fewer studies focused on miRNAs related to a cluster of genes regulating thyroid hormone synthesis, such as NIS, Pendrin, TPO, MCT8, TSHR, TSHα, and TSHß-related miRNAs in structural and functional changes of the thyroid gland induced by subchronic and chronic high iodine exposure. In the present study, one hundred and twenty 4-week-old female Wistar rats were randomly divided into control group (I50µg/L KIO3); HI 1 (I6000µg/L KIO3); HI 2 (I10000µg/L KIO3); and HI 3 (I50000µg/L KIO3), the exposure period was 3 months and 6 months, respectively. The iodine contents in the urine and blood, thyroid function, and pathological changes were determined. In addition, levels of thyroid hormone synthesis genes and the associated miRNAs profiling were detected. The results showed that subclinical hypothyroidism occurred in the high iodine groups with subchronic high iodine exposure, while 6-month exposure led to hypothyroidism in the I10000µg/L and I50000µg/L groups. Subchronic and chronic high iodine exposure caused mRNA and protein levels of NIS, TPO, and TSHR decreased significantly, and Pendrin expression increased significantly. In addition, MCT8 mRNA and protein levels are only remarkably decreased under the subchronic exposure. PCR results showed that levels of miR-200b-3p, miR-185-5p, miR-24-3p, miR-200a-3p, and miR-25-3p increased significantly exposed to high iodine for 3 months, while miR-675-5p, miR-883-5p, and miR-300-3p levels increased significantly under the exposure to high iodine for 6 months. In addition, miR-1839-3p level was markedly decreased exposed to high iodine for 3 and 6 months. Taken together, the miRNA profiling of genes regulating thyroid hormone synthesis remarkably altered from subclinical hypothyroidism to hypothyroidism induced by excess iodine exposure, and some miRNAs may play an important role in subclinical hypothyroidism or hypothyroidism through regulating NIS, Pendrin, TPO, MCT8, and TSHR providing promising targets to alleviate the impairment on the structure and function of thyroid gland.

Association between different water iodine exposures and thyroid cancer: A retrospective study of high water iodine areas in China from 2009 to 2020.

In recent years, the incidence of thyroid cancer has been on a significant rise worldwide, and a number of environmental factors have been suspected to be risk factors for thyroid cancer, especially the relationship between iodine intake and thyroid cancer has attracted attention. In this study, we want to assess the relationship between different water iodine exposures and thyroid cancer incidence before and after water alteration in areas with high water iodine in China. Thyroid cancer patients (2009-2020) were enrolled at two hospitals, both in Heze City, Shandong Province, an area with high water iodine levels. According to the criteria of the study, 5826 cases out of 8785 cases were selected for inclusion in the study. Before and after water alteration, the incidence of thyroid cancer was highest in areas with water iodine concentrations of 200-300 µg/L in high iodine areas. In areas where water iodine decreased to adequate iodine levels, there was a strong negative correlation between the decreased level of water iodine and the incidence of thyroid cancer. In addition, in cases with pathology reports, we found that the greater the decrease in water iodine values, the markedly smaller the maximum diameter of the thyroid cancer lesions. Taken together, these findings suggest that we should continue to monitor the incidence of thyroid cancer in areas with high water iodine and continue to optimize population iodine intake to reduce the incidence of thyroid cancer.