The relation of adiponectin and tumor necrosis factor alpha levels between endothelial nitric oxide synthase, angiotensin-converting enzyme, transforming growth factor beta, and tumor necrosis factor alpha gene polymorphism in adrenal incidentalomas.

OBJECTIVE: The aim of our study was to demonstrate demographic characteristics, presence of inflammatory markers, distribution of angiotensin-converting enzyme (ACE), tumor necrosis factor (TNF), endothelial nitric oxide synthase (eNOS) genotypes and relations among these parameters in these patients and control subjects. RESEARCH DESIGN AND METHODS: Study samples were collected from 50 patients with adrenal mass and 30 control groups. The eNOS, ACE, TNF-alpha, transforming growth factor (TGF)-beta genes polymorphisms, TNF-alpha, adiponectin levels were analysed in 50 unrelated Turkish patients with a diagnosis of adrenal incidentaloma (AI). RESULTS: There was statistically significant difference between TNF-alpha levels of patient and controls (p=0.048). We have not detected the connection between TGF-beta, TNF-alpha, ACE, eNOS gene polymorphism with serum TNF-alpha and adiponectin levels. In this study, we demonstrated that there were significant differences for ACE genotypes in the patients when compared to the controls (p<0.05). The percentages of the ID, DD, II genotypes for ACE gene polymorphism in the patients group were 30.0, 13.0, 7.0%, respectively. CONCLUSIONS: According to different cases of eNOS, TGF-beta, ACE, and TNF-alpha gene genotypes; no statistical significant difference was found between basal cortisol, ACTH, DHEAS, metanephrine, renin, aldosterone, normetanephrine, 17-hydroxyprogesterone, 1 mg low-dose dexamethasone suppression test-cortisol response and AI size. In this study, I/D genotype was determined to be statistically higher in ACE gene in patients with AI (p=0.014).

Oxidative stress markers in young patients with polycystic ovary syndrome, the relationship between insulin resistances.

OBJECTIVE: Polycystic ovary syndrome is a syndrome of ovarian dysfunction. Oxidative stress, inflammation and endothelial cell activation are thought to play concomitant roles in the pathogenesis of the above diseases particularly in the development of atherosclerotic lesions. RESEARCH DESIGN AND METHODS: We studied 58 polycystic ovary syndrome patients and age-matched 25 healthy controls consisting of women that have regular, ovulatory cycles and normal androgen levels. Homeostasis Model Assessment-Insulin Resistance for this study was taken as 1.75 that is the upper level of confidence interval of %95 of the mean of the healthy group. PCOS patients were divided into two groups as for below the cut-off level (<1.75) and above the cut-off level (> or =1.75). hs-CRP, fibrinogen, malondialdehyde, nitric oxide and disulfide level results were compared both in PCOS and control groups. RESULTS: In this study, sensitive CRP was found to be statical significantly higher in polycystic ovary syndrome groups whose Homeostasis Model Assessment-Insulin Resistance were > or =1.75 and <1.75 when compared to the control group. But, no significantly correlation was determined between malondialdehyde, nitric oxide and disulfide levels and CRP elevation. CONCLUSIONS: In our study, because those participants were young and non- obese patients with PCOS, malondialdehyde, nitric oxide and disulfide levels and Carotid Artery Intima-Media Thickness measurements as a pre-indicator of cardiovascular disease were not found to be different from those of the controls.

Polymorphism of the interleukin-10 gene in polycystic ovary syndrome.

Interleukin (IL)-10 is a major anti-inflammatory cytokine that has been associated with obesity and type 2 diabetes. We aimed to evaluate the IL-10 gene polymorphisms in polycystic ovary syndrome (PCOS) and control subjects. Ninety-one young women with PCOS and 74 healthy control women were included in our study. All subjects underwent venous blood drawing for complete hormonal assays, lipid profile, glucose, insulin and IL-10 gene polymorphism genetic analysis and carotid intimae media thickness (CIMT) were measured. The genotype and allele frequencies showed similar ratios between both the control and the patient group. The AA and AG genotypes in IL-10 polymorphism seemed to be relatively high, but statistically no significant difference has been detected in GG genotype. Our results show that IL-10 gene polymorphism of PCOS patients has no effect on inflammatory markers, metabolic parameters (fasting insulin, fasting glucose, HOMA-IR), carotid intimae media thickness and Ferriman- Gallwey scoring. These data will be different in PCOS patients with different ethnical origin.

Increased oxidative DNA damage in lean normoglycemic offspring of type 2 diabetic patients.

OBJECTIVE: Several studies have shown increased oxidative stress in patients with pre-diabetes and newly diagnosed Type 2 diabetes mellitus (T2DM). It has been proposed that oxidative stress initiates insulin resistance in genetically predisposed individuals. The aim of this study was to evaluate the markers of oxidative stress in the offspring of patients with T2DM. MATERIAL AND METHODS: We examined 60 lean normoglycemic offspring of Type 2 diabetics, and 52 age, sex and body mass index matched subjects without family history of T2DM as controls. Anthropometric, biochemical and carotid intima media thickness (IMT) measurements and oral glucose tolerance test (OGTT) were performed. Erythrocyte superoxide dismutase and glutathione peroxidase activities, serum nitric oxide, plasma total sulfhydryl (tSH) groups, plasma total antioxidant status, plasma malondialdehyde and serum 8-hydroxydeoxy-guanosine (8-OHdG) levels were compared between 2 groups. RESULTS: 2 groups were similar for the measurements of anthropometric, blood pressure, lipids, fasting glucose, HOMA-IR and carotid IMT. Glucose levels during OGTT were significantly higher in the offspring of Type 2 diabetics than controls (p=0.035). The offspring of Type 2 diabetics showed a significant increase in serum 8-OHdG level (p=0.005) and plasma tSH groups (p=0.032) when compared to the controls. Significant differences were not obtained in other oxidative stress marker levels between 2 groups. CONCLUSION: Main finding of our study was the presence of increased oxidative DNA damage in lean normoglycemic offspring of Type 2 diabetic patients. There is a need for further clinical studies in order to explain whether oxidative stress is present in genetically predisposed subjects and induces the insulin resistance.

Human multidrug resistance-1 gene expression levels in graves-basedow disease.

OBJECT: Multidrug resistance 1 gene is responsible for the resistance of a large variety of drugs in human cells. We tried to evaluate this in the present study in thyroid stimulant hormone receptor antibody positive subjects. METHOD: In study enrolled 23 female and 10 male subjects. Hyperthyroid subjects were treated with PTU and remission was assured between 6-12 months. Blood samples were collected before the start of this treatment. Permission for this study was taken from the patients and the local ethical committee. RESULTS: Serum F-T3, F-T4 levels in Graves subjects were markedly high, whereas TSH levels were markedly low than normal range. We also found that with increased age of the Graves' subjects, MDR-1 gene expression decreased. There was also a direct correlation between blood MDR-1 gene expression and TSH-R Ab levels in patients with Graves's disease. We observed that the duration of being euthyroid was lengthened with the elevation of MDR-1 gene expression. There was a direct correlation between blood MDR-1 gene expression levels and ultrasonografic size of thyroid gland. CONCLUSION: As a result, raised blood MDR-1 gene expression levels in patients with Graves-Basedow disease may be associated with the activity of the disease and the resistance to its treatment. The more blood MDR-1 expression increases the more the duration of being euthyroid increases.