No abstract

Objective To determine the characteristics of thyroid nodules by using fine needle aspiration (FNA)

Insulin resistance is one of the feature of obesity. Fetuin A is inhibitor of insulin receptor which belongs the family of receptor tyrosine kinase. It has been observed that fetuin-null mice are resistant to diet-induced obesity and they exhibit increased insulin sensitivity. Increased production of reactive oxygen species is suggested to be associated with insulin resistance. Attacks of reactive oxygen species to DNA results in base oxidation. Among the oxidized bases, 8-hydroxydeoxyguanosine is predominant lesion with pro-mutagenic potential. In the present study; measurement of serum levels of fetuin A and 8-hydroxydeoxyguanosine in obese subjects (n=46) and healthy controls (n=22), and examination of the relations between these parameters and insulin resistance have been purposed. Blood samples were taken form morbidly obese subjects after a 12 h fasting. Serum levels of fetuin A and 8-hydroxydeoxyguanosine were measured by ELISA. Statistical analysis was performed by Mann Whitney U test and correlations were examined by Spearman correlation coefficient. Serum levels of total cholesterol, HDL, LDL, VLDL, triglycerides, free T3, free T4, fasting glucose, c-peptide and %HbA1c in the obese group were found to be different from those in the control group. Serum level of fetuin A was found to be higher, 8-hydroxydeoxyguanosine level was found to be lower in the morbid obese group than those in the control group. Fetuin A was found to be positively correlated with HOMA-IR (r:0,40, P<0.05) and negatively correlated with 8-hydroxydeoxyguanosine (r:-0,52, P<0.01). No significant association was determined between body mass index and measured parameters. In conclusion, serum level of fetuin A is high in morbidly obese subjects and is negatively associated with 8-hydroxydeoxyguanosine level in peripheral circulation. Fetuin A may be a promising link between insulin resistance and obesity as well its comorbidities.

Objective: To compare glutathione S-conjugate transport in obese and nonobese persons, and how glutathione S-conjugates are involved in the antioxidant status in obesity. Materials and methods: The efflux of glutathione conjugates and malondialdehyde (MDA) levels were measured in erythrocytes of obese (N ¼ 33) and nonobese (N ¼ 28) persons at every 30 min during a 120 min incubation time in vitro. 2,4-dinitrophenyl-S-glutathione (DNP-SG) represented the glutathione S-conjugate. Results: The efflux of conjugate in erythrocytes from obese subjects (7087147 DNP-SG efflux nmol/ml erythrocytes/h) was significantly higher than that of control group (4907105 DNP-SG efflux nmol/ml erythrocytes/h) (Po0.05). At all time points measured (30-120 min), there was an increase in DNP-SG efflux in obese group (Po0.05). This is manifested by a decrease in cellular DNP-SG levels. The susceptibility of erythrocytes to in vitro 1-chloro-2,4-dinitrobenzene (CDNB)-induced oxidative stress were greater for cells of control group (Po0.05), although hemolysis sensitivity of these cells are not different between both groups (P40.05). Following CDNB pretreatment, incubation of erythrocyte with vanadate, a DNP-SG transport inhibitor, resulted in an increase of MDA in both groups. However, in this case, the difference in susceptibility was not related to obesity. On the other hand, while erythrocyte glutathione level was lower in obese subjects (79% of control) than in controls (Po0.05), the adenosine 5 0 -triphosphate (ATP) levels, the enzyme activities of glutathione S-transferase (GST) and the conjugation capacities of the erythrocytes were not different between groups (P40.05). Conclusion: Obesity may increase erythrocyte glutathione conjugate transport independent from ATP and GST activity that may protect against MDA formation in vitro.

The relationship between autoimmune thyroiditis and systemic sclerosis is controversial. Data exist on the presence of thyroid autoantibodies in patients with systemic sclerosis but, as far as we could ascertain, anti-Scl-70 antibodies, which are highly specific for systemic sclerosis, have not been investigated in autoimmune hypothyroidism. This study compares the presence of anti-Scl-70 in females with autoimmune hypothyroidism (n = 24) and in healthy age-matched female controls (n = 26). Free thyroxine levels were similar in both groups. Thyroid stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), antithyroglobulin (anti-Tg) and index values for anti-Scl-70 levels were significantly higher in patients with autoimmune hypothyroidism compared with controls, although the anti-Scl-70 test was negative in both groups. Anti-TPO, anti-Tg and TSH significantly correlated with anti-Scl-70. In conclusion, autoimmune hypothyroidism seems to be associated with a higher index level of anti-Scl-70, yet a negative anti-Scl-70 antibody test. This suggests that autoimmune hypothyroidism might have common aetiological factors with systemic sclerosis.