ACTA ENDOCRINOLOGICA (BUC)

Background. Thyroid dysfunction during pregnancy may adversely affect mother and fetus. A number of disorders\r\nhave been described as a cause of thyrotoxicosis in pregnancy. Subacute thyroiditis is a rare cause of thyrotoxicosis in pregnant women. Although self limited, due\r\nto both hyper- and subsequent hypothyroidism, this disorder may have deleterious effects in outcome of pregnancy.\r\nCase report. A 29 year old woman in the first trimester of pregnancy was referred due to palpitation, malaise and pain in thyroid region. Laboratory data revealed a suppress TSH, elevated Free T4 and high ESR. Pregnancy test was positive. Diagnosis of subacute thyroiditis was made by Doppler\r\nsonography of thyroid. A dramatic response to prednisolone was observed. Two months later because of hypothyroidism,\r\nlevothyroxine was started and continued throughout pregnancy. She delivered a healthy baby at term without complication.\r\nConclusions. Although subacute thyroiditis is rare during pregnancy, its possibility should be kept in mind in hyperor\r\nhypothyroid pregnant women.

Background. Resistin, as an adipokine, has been shown to be increased in serum plasma of gastric cancer patients and suggested to be a major factor in gastric carcinogenesis. However, it is still not clear how Resistin influences gastric cancer progression. The aim of this study was to evaluate Resistin effect on cell proliferation and expression of telomerase gene in gastric cancer cell line (AGS). Methods. In this study, the proliferating activity of AGS cells stimulated with Resistin was also evaluated by using 2,3-Bis-(2-Methoxy-4-Nitro-5-Sulfophenyl)-2HTetrazolium- 5-Carboxanilide (XTT) assay and trypan blue staining method. To investigate telomerase gene expression affected by Resistin, total RNA was extracted, cDNA was synthesized and expression of hTERT mRNA was carried out by real-time reverse transcription polymerase chain reaction. Results. Exogenous Resistin has induced gastric cancer cells proliferation in a dose-dependent manner and could improve cell viability. Also the expression of Human Telomerase Reverse Transcriptase (hTERT) was upregulated in 24 hours, after Resistin treatment. Conclusions. This study has shown Resistin induces exogenously gastric cancer cell proliferation and increases hTERT gene expression. These findings may clarify the role of Resistin in gastric carcinogenesis. Therefore blocking Resistin signaling and limiting its secretion may be valuable for the treatment of gastric cancer.

Methods. Ninety Wistar male rats were used in this study. Type 1 diabetes was induced by i.p injection of 50 mg/kg of streptozotocin in all animals. After 42 days of treatment with testosterone (2mg/kg/day) or voluntary exercise alone or in combination, the heart of the rats has been removed and MicroRNA was extracted from the heart using miRCURYTM RNA isolation kit. Results. Our results showed that either testosterone or exercise increased miRNA-126 expression levels in the heart of diabetic rats. Treatment of diabetic rats with testosterone and exercise at the same time had a synergistic effect on miRNA-126 levels in the heart. Furthermore, in castrated diabetes group, miRNA-126 levels were significantly decreased in heart, whereas either testosterone treatment or exercise training enhanced expression of this miRNA. Also, simultaneous treatment of castrated diabetic rats with testosterone and exercise had an additive effect on miRNA-126 expression levels. Conclusion. This study showed that testosterone and exercise promote an increase in the expression of miRNA-126 in the heart tissue and this may be related to cardiac angiogenesis. These results may indicate that testosterone and exercise can help to prevent progression of diabetic cardiomyopathy due to impaired angiogenesis in the heart.

important role in insulin signaling and the common Gly971Arg polymorphism is related to type 2 diabetes (T2D). IRS-1 Gly971Arg polymorphism can modify tyrosine phosphorylation at a specific site of IRS-1 and may have a critical role in the development of insulin resistance (IR). Objective. The purpose of this study was to investigate the association between this polymorphism and IR in Iranian patients with newly-diagnosed type 2 diabetes. Design. The study was conducted on 114 individuals with newly-diagnosed T2D and 118 healthy matched controls, aged 20-80 years. Fasting blood glucose and insulin were measured by the enzymatic method and enzyme-linked immunosorbent assay, respectively. Insulin-resistance was calculated by homeostasis model assessment estimatedinsulin resistance (HOMA-IR). The gene polymorphism was examined by polymerase chain reaction-restriction fragment length polymorphism. Results. There are significant differences between IRS1 Gly971Arg polymorphism and studied individuals (P<0.0001). The findings showed that the risk of developing T2D in individuals who had R-alleles was 3.74 folds higher than those without R-alleles. However, IRS1 Gly971Arg polymorphism was not associated with high HOMA-IR, high BMI and familial history of diabetes. Conclusions. Even though there was not a significant relationship between IRS-1 G971R polymorphism with insulin resistance and high BMI, this polymorphism was correlated to newly-diagnosed diabetic patients. Thus, the evaluation of IRS-1 G971R polymorphism may be helpful for predicting T2D new cases.