ACTA ENDOCRINOLOGICA (BUC)

Context. Thyroid eye disease (TED), an orbital inflammatory status, generally occurred in Graves’ disease. Objective. This study aimed to acquire further insight into molecular mechanisms of TED, especially several key involved genes and pathways. Design. The microarray dataset GSE58331 including expression data for orbital adipose tissue samples, isolated from TED patients and normal controls, was downloaded from a publicly accessible Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified from 23 adipose tissues of TED patients versus 20 samples from normal controls. Subjects and Methods. A protein-protein interaction network of DEGs was constructed by using Search Tool for the Retrieval of Interacting Genes and Cytoscape 3.6.0. Several hub genes/proteins were extracted from the proteinprotein interaction network based on connectivity degree. Furthermore, we used the iRegulon plugin of Cytoscape3.6.0 to predict the transcription factors (TFs). Results. A total of 678 DEGs (538 up- and 140 down-regulated genes) were identified in TED patients. Proopiomelanocortin (POMC), interleukin 2 (IL-2), G protein subunit gamma 3 (GNG3), CXC motif chemokine receptor 4 (CXCR4), toll like receptor 4 (TLR4), colony stimulating factor 1 receptor (CSF1R), lysophosphatidic acid receptor 3 (LPAR3), CXC motif chemokine ligand-8 (CXCL8), etc., were considered as the hub genes among the DEGs. There were 6 TFs predicted to be differentially expressed in regulating the DEGs related to TED. A total of 71 DEGs had been reported to be associated with TED in the Comparative Toxicogenomics Database. Conclusions. Through this analysis, we have identified plenty of potential biomarkers and pathways which may have an important role in the pathogenesis of TED. However, these findings require verification by more detailed future experimental studies.

Radioactive iodine (RAI) therapy is a mainstay adjuvant treatment for thyroid cancer. Administration of RAI therapy after total or near-total thyroidectomy has shown a survival advantage in numerous properly selected patients. However, the role of RAI therapy after reoperation for persistent or recurrent differentiated thyroid carcinomas (DTCs) is unclear. One reason may be the possible downregulation of the I- transport system after primary surgery. RAI is transported by the sodium iodide symporter (NIS), PENDRIN, anoctamin 1 (ANO1) and cystic fibrosis transmembrane conductance regulator (CFTR) and emits β particles that destroy follicular cells. The identification of pathways of iodide (I-) transport has allowed use of the transport system to render tumours susceptible to RAI treatment via gene therapy. This review focuses on the effect of RAI therapy in follicular cell-derived thyroid cancers and offers potential novel targets that enable improved radioiodine uptake and thus an improved prognosis of thyroid cancer.

Objective. To observe the effect of adiponectin on osteogenesis in type 2 diabetic rats. Methods. The 4th-week-old male SD rats were divided into normal control group (n=18) and diabetic model group (n = 42). Type 2 diabetes was induced by high-fat and high-sugar diet and intraperitoneal injection of a low dose of streptozotocin (STZ). The successfully-induced diabetic rats were divided into diabetic group (DM=18) and adiponectin intervention group (APN=18). APN group was injected with APN 10 μg/kg*d. The rats were separately sacrificed at the 4th, 8th and 12th week after the intervention. Bone microstructure and adipose tissue were observed via HE staining. Bone marrow was extracted from one side of the femur, and the supernatant was achieved by centrifugation. After BMD assessed by DXA, the other side of the femur was for further HE staining. Runx-2 expression in the bone marrow cells was detected by RT-PCR. BALP and AOPPs in bone marrow supernatant were assayed by ELISA. AGEs were detected by immunohistochemical staining. Results. With the feeding time over, blood glucose, AOPP, and AGEs were increased, and Runx-2 mRNA, BALP, BMD were decreased in diabetic rat group(P<0.05). Oxidative stress (OS) maker (AOPP) was decreased and osteogenesis makers (Runx2 mRNA, BALP) were increased after intervention with exogenous adiponectin (P<0.05). At the 8th and 12th week, the trabecular bone became thinner and broken, and the fat cell number increased in all 3 groups, especially in the DM group. The adiponectin intervention group showed that the trabecular bone structure was moderately restored. Conclusions. OS is obvious in bone microenvironment in diabetic rats. OS may have an inhibitory effect on regulation of osteogenic differentiation factor Runx2, causing down regulation of osteoblast differentiation and bone formation. Adiponectin may improve OS response and protect the bone structure.

Background. To evaluate iodine status and the prevalence of thyroid disorders in different populations of Zhoushan Island, China.\r\nMethods. A total of 3284 inhabitants of Zhoushan Island were surveyed, including 1389 urban residents, 737 salt workers, 502 peasants, 362 fishermen, and 294 monks from Mount Putuo. All subjects, except for salt workers, consumed iodized salt. A thyroid ultrasound was performed and serum levels of\r\nthyroid hormones and thyroid peroxidase antibody were measured.\r\nResults. The median urinary iodine concentration was significantly higher in subjects who consumed iodized salt than in those who consumed non-iodized salt. No significant differences were noted in the prevalence of thyroid ultrasound abnormalities and functional thyroid disorders between subjects who consumed non-iodized and iodized salt except between salt workers and monks from Mount Putuo. The prevalence of thyroid ultrasound abnormalities differed\r\nsignificantly between males and females and was positively correlated with advanced age (r=0.212, P<0.001).\r\nConclusions. Iodine intake is considered adequate, more than adequate, or excessive amongst the study populations. The\r\nprevalence of both thyroid ultrasound abnormalities and functional thyroid disorders is extremely high in Zhoushan Island. Advanced age and female gender are significant predictors of thyroid ultrasound abnormalities.

Aim. To explore the effects and underlying mechanisms of pioglitazone (pio) on insulin sensitivity in insulin-resistant KKAy mice. Methods. Sixteen eight-week-old male KKAy mice were randomly assigned to two groups based on body weight: an insulin resistance model group and a pioglitazone treatment group (hereafter referred to as the pio-group). Eight male C57BL/6J mice were used as an insulin resistance control group. Mice in all three groups were fed an AIN-93G diet, and pio was added to the diet in the pio-group. After twelve weeks of treatment, blood glucose, serum insulin, glucose tolerance, and insulin tolerance were measured. ELISA was used to determine adiponectin and leptin in serum. A real time PCR assay was used to detect the mRNA of adiponectin and leptin in epididymal adipose tissue. A Western blot assay was used to analyze protein expression and/ or phosphorylation levels of peroxisome proliferator activated receptor γ (PPARγ), insulin receptor substrate 1 (IRS1), and protein kinase B (PKB/AKT) in the liver and epididymal adipose tissue.Results. The results showed that Pio treatment may effectively reduce levels of blood glucose and serum insulin, improve insulin tolerance and glucose tolerance, increase serum adiponectin, decrease serum leptin, and enhance mRNA expression of adiponectin in epididymal adipose tissue. Furthermore, with pio treatment, protein expression of PPARγ and phosphorylation levels of IRS1 and AKT were increased in the liver and epididymal adipose tissue. Conclusion. These results suggested that Pio intervention may ameliorate insulin resistance and improve insulin sensitivity in KKAy mice, which may be due to an increase of PPARγ and further activation of the insulin signaling transduction pathway (IRS1 and AKT) in the liver and epididymal adipose tissue of KKAy mice.