Anti-Human Thyroglobulin monoclonal antibody

The presence of autoimmune thyroid condition could lead to thyroid dysfunction in adults. In addition, thyroid antibody positivity has been suggested to be associated with hyperuricemia, diabetes and obesity in individuals with thyroid autoimmune diseases. Currently, there are limited studies that assessed the relationship of thyroid antibody with the components of metabolic syndrome in adults, especially from iodine-sufficient regions. Therefore, the aim of this study was to determine the prevalence of components of metabolic syndrome in Chinese adults with autoimmune thyroid condition. Medical records of adult inpatients in the Suzhou Ninth People's Hospital, Suzhou, Jiangsu, China, from January 2016 to September 2019 were reviewed and included after screening for eligibility. A total of 1105 participants were included in our final analysis, and of these, 77.5% (n= 856) were females. There was a higher prevalence of thyroid antibodies in females than males (30.6% vs. 23.7%) (p= 0.034). Although there were significant differences in mean TSH, FT3 and FT4 values between participants positive and negative for thyroid antibodies, these values were still within the normal reference range. No differences in the mean BMI, prevalence of diabetes, hyperuricemia, hypertriglyceridemia and hypercholesterolemia between participants positive and negative for thyroid antibodies were reported (p> 0.05). In conclusion, our study reported that participants positive for thyroid antibodies did not appear to be accompanied by abnormal thyroid function, lipid profile, uric acid and glucose concentrations.

Background: Thyroid hormone (TH) synthesis is essential for the control of development, growth, and metabolism in vertebrates and depends on a sufficient dietary iodine intake. Importantly, both iodine deficiency and iodine excess (IE) impair TH synthesis, causing serious health problems especially during fetal/neonatal development. While it is known that IE disrupts thyroid function by inhibiting thyroid gene expression, its effects on thyroid development are less clear. Accordingly, this study sought to investigate the effects of IE during the embryonic development/differentiation of endoderm and the thyroid gland. Methods: We used the murine embryonic stem (ES) cell model of in vitro directed differentiation to assess the impact of IE on the generation of endoderm and thyroid cells. Additionally, we subjected endoderm and thyroid explants obtained during early gestation to IE and evaluated gene and protein expression of endodermal markers in both models. Results: ES cells were successfully differentiated into endoderm cells and, subsequently, into thyrocytes expressing the specific thyroid markers Tshr, Slc5a5, Tpo, and Tg. IE exposure decreased the messenger RNA (mRNA) levels of the main endoderm markers Afp, Crcx4, Foxa1, Foxa2, and Sox17 in both ES cell-derived endoderm cells and embryonic explants. Interestingly, IE also decreased the expression of the main thyroid markers in ES cell-derived thyrocytes and thyroid explants. Finally, we demonstrate that DNA methyltransferase expression was increased by exposure to IE, and this was accompanied by hypermethylation and hypoacetylation of histone H3, pointing to an association between the gene repression triggered by IE and the observed epigenetic changes. Conclusions: These data establish that IE treatment is deleterious for embryonic endoderm and thyroid gene expression.