Senay Topsakal

Relation with HOMA-IR and thyroid hormones in obese Turkish women with metabolic syndrome

The aim of this study was to investigate the relationship between insulin resistance and thyroid function in obese pre- and postmenopausal women with or without metabolic syndrome (MetS). 141 obese women were divided into two groups, HOMA-IR<2.7 and HOMA-IR>2.7, to evaluate relation with HOMA-IR and fatness, hormone and blood parameters. They were then divided into four groups as pre- and postmenopausal with or without MetS. Various fatness, hormone and blood parameters were examined. Statistically significant difference was found in weight, body mass index (BMI), waist circumference, fat%, fasting insulin, TSH, FT3, FT4, FSH, Anti-microsomal antibody (ANTIM) and triglycerides levels in HOMA-IR<2.7 and HOMA-IR>2.7 obese Turkish women. This study showed that age, weight, BMI, waist circumference, fat%, fasting insulin, FT3, ANTIM, FSH, LH, total cholesterol, triglycerides, HDL, HOMA-IR, systolic and diastolic blood pressure levels were related in preand post menopausal status in obese women with or without MetS. Obesity may influence the levels of thyroid hormones and increases the risk of MetS in women. Postmenopausal status with MetS is associated with an increased TSH, FT3 and FT4 levels and HOMA-IR in obese women. Strong relation was observed with MetS and TSH and FT3 levels.

Early degenerative effects of diabetes mellitus on pancreas, liver, and kidney in rats: an immunohistochemical study.

Liver and kidney commonly affected by diabetes in chronic cases but pathogenetic mechanisms are not fully understood in early stages of the disease. The aim of this study was to investigate the immunohistochemical expression of caspase-3, cyclooxygenase (COX)-1 and-2, calcium sensing receptor (CSR), and hypoxia inducible factor-1α (HIF-1α) in pancreas, liver, and kidney in streptozotocin (STZ) induced DM. Study group (n = 6) were received streptozotocin (50 mg/kg) and control group (n = 6) physiologic saline. The blood glucose and ketonuria were measured, and necropsy was performed on them on third, fourth, and fifth days. Immunohistochemistry revealed that marked increase in caspase-3 reaction pancreas, liver, and kidney in the study group than control group. COX-1 slightly increased in these organs in study group compared to controls. Immunohistochemically COX-2 reaction was markedly positive in liver and kidney, but slightly increased in pancreas. The most increased reaction was observed in CRS and all organs were markedly positive. HIF-1α expression was also increased but the reaction was more severe in pancreas than liver and kidney. This study indicated that degeneration starts in organs in early stages of the disease and the most effective route for degeneration related to increase of calcium influx and hypoxia upon cells in DM.

Association of serum lipid levels with diabetic retinopathy.

AIM To assess the association between serum lipids and diabetic retinopathy (DR). METHODS Sixty-one diabetic patients without retinopathy(NDR), 55 diabetic patients with non-proliferative retinopathy(NPDR) and 75 diabetic patients with proliferative retinopathy (PDR) according to ETDRS grading scale were enrolled in this study. Total cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL) and triglyceride values were compared between the groups. RESULTS The groups were well-balanced in terms of age and gender (P=0.071, P=0.265 respectively). The mean HbA1c values were significantly lower in NDR group than the NPDR and PDR groups (P=0.004, P=0.009 respectively). Mean total cholesterol, triglyceride, LDL, HDL and VLDL levels were not significantly different between the groups (P=0.693, P=0.774, P=0.644, P=0.910 and P=0.967 respectively, one way ANOVA). Mean total cholesterol, triglyceride, LDL, HDL and VLDL levels were not significantly different between the patients with ME and patients without ME (P=0.622, P=0.113, P=0.955, P=0.735 and P=0.490 respectively, t-test). The mean blood glucose significantly correlated with total cholesterol (r=0.173, P=0.017) and LDL (r=0.190, P=0.008). The mean HbA1c significantly correlated with total cholesterol (r=0.158, P=0.030) and triglyceride (r=0.148, P=0.042). CONCLUSION Serum lipid levels were not significantly associated with the severity of DR or existence of ME despite the significant correlation between the mean blood glucose, HbA1c and total cholesterol.

Effects of etanercept on sodium taurocholate-induced acute pancreatitis in rats

In this study, we examined the effects of etanercept (ETA) on experimentally induced pancreatitis. Acute pancreatitis was induced with Na taurocholate. ETA was simultaneously administered to treatment groups. Serum amylase and lipase activity, pancreatic histopathology, apoptosis, malondialdehyde (MDA), and myeloperoxidase enzyme activity (MPO) were assessed. Although rats in the groups 1, 2, and 3 were sacrificed 24h later, groups 4, 5, and 6 were sacrificed 5 days later. ETA treatment significantly decreased serum amylase activity (nontreated, 2636.16+/-191.94; treated, 1898.71+/-262.53; control, 506.28+/-17.31 U/L, P<0.001), lipase activity (nontreated, 3049.67+/-972.65; treated, 2538.85+/-660.45; control, 88.57+/-7.54 U/L, P<0.001), histopathologic score (nontreated, 5.43+/-0.43; treated, 2.57+/-0.20; control, 0.71+/-0.18, P<0.001), MDA (nontreated, 105.77+/-13.29; treated, 92.89+/-10.39; control, 41.26+/-2.54 nmol/g, P<0.001), and MPO (nontreated, 0.64+/-1.15; treated, 0.59+/-0.13; control, 0.17+/-0.02 units/g/wet weight, P<0.001) activity in 24-h groups. In 5-day groups, ETA treatment decreased amylase activity (nontreated, 738.67+/-48.60; treated, 497.14+/-47.25; control, 389.00+/-9.17 U/L, P<0.001), lipase activity (nontreated, 101.33+/-39.32; treated, 34.57+/-7.29; control, 23.42+/-2.12 U/L, P<0.001), histopathologic score (nontreated, 5.43+/-0.43; treated, 3.71+/-0.68; control, 0.00+/-0.00, P<0.001), MDA (nontreated, 67.91+/-4.28; treated, 60.91+/-3.57; control, 14.85+/-1.16 nmol/g, P<0.001), and MPO (nontreated, 0.36+/-0.04; treated, 0.27+/-0.02; control, 0.14+/-0.02 units/g/wet weight, P<0.001) activity. Caspase-positive cells numbers around the necrosis significantly decreased by ETA treatment in both 24-h groups (nontreated, 74.28+/-3.26; treated, 67.00+/-1.15; control, 3.85+/-0.63, P<0.001) and 5-day groups (nontreated, 79.85+/-3.01; treated, 47.85+/-5.76; control, 2.22+/-0.63, P<0.001). These results showed that ETA has an ameliorating effect on sodium taurocholate-induced acute necrotic pancreatitis.

Effects of Caffeine and Lycopene in Experimentally Induced Diabetes Mellitus.

Objectives Diabetes mellitus (DM) is a global epidemic with increasing prevalence. The disease is chronic in nature, and patients must use antidiabetic drugs or insulin during their lifespan. Because of the difficulty of using injectable insulin preparations, patients and practitioners prefer to use oral antidiabetic drugs for prophylaxis and treatment. There are, however, numerous adverse effects of antidiabetic drugs and rapidly increasing attention is being paid to new nutraceutical drugs with fewer adverse effects. The purpose of this study was to evaluate the effects of caffeine and lycopene on streptozotocin (STZ)-induced DM in rats. Methods Caffeine and lycopene were administered to the study groups by oral gavages for 1 month whereafter experimental diabetes was induced in 90 rats in 6 groups. Results There were no pathological effects of lycopene and caffeine on the pancreas. Marked vacuolization and degeneration were observed in STZ-treated groups. Caffeine and lycopene decreased the pathological findings and lowered the blood and urine glucose levels in the rats with STZ-induced DM, whereas these compounds increased serum insulin levels. Conclusions This study showed that caffeine and lycopene provided protective effects against experimentally induced DM. The protective effects of lycopene were observed to be much greater than those of caffeine.

Effect of Insufficient Insulin Treatment in Streptozotocin-induced Diabetes Mellitus

Objectives: In this study, we investigated clinically, pathologically, and immunohistochemically the effect of insufficient short-acting insulin treatment on streptozotocin (STZ)-induced diabetes mellitus in rats. Methods: Three groups composed of 10 rats each were studied as follows: (1) a group that received only STZ (50 mg/kg) (STZ group); (2) a group that received 50 mg/kg STZ and, after 12 hours, 8 IU of short-acting insulin treatment (STZ + INS group), repeated every night for 5 days; and (3) a control group. Ketonuria and blood glucose levels were examined every day. Blood was obtained from 2 rats from each group, and necropsy was performed every day during the 5-day period. Results: Hyperglycemia was observed in the STZ and STZ + INS groups 24 hours after, but levels were higher in the STS + INS group than those in the STZ-only group. Histopathology was similar in the STZ and STZ + INS groups, and degeneration was observed in both groups, but immunohistochemistry revealed a more severe reduction in insulin-secreting cells in the STZ + INS group than that in the STZ group. There were no hyperglycemia and histopathological or immunochemical alteration in the control group. Conclusions: This study showed that insufficient short-acting insulin treatment can increase the diabetogenic effect of STZ in rats.

Relationship of apelin, procalcitonin, and fetuin-A concentrations with carotid intima-media thickness in acromegaly

Background Acromegaly is characterized by excess growth hormone and insulin-like growth factor-1 concentrations. There is conflicting evidence as to whether acromegaly is associated with an increased risk of atherosclerosis. Apelin is an adipose tissue-derived peptide that may be associated with hyperinsulinemia. Fetuin-A is a hepatocyte produced plasma glycoprotein that has an important role as a calcification inhibitor. The aim of this study was to examine apelin, fetuin-A, and procalcitonin concentrations and to assess their relationship with carotid intima medial thickness (cIMT) in subjects with acromegaly. Methods Apelin, fetuin-A, and procalcitonin serum concentrations were measured in 37 (20 inactive and 17 active) subjects with acromegaly and 30 control subjects, along with carotid intima medial thickness. Results The concentrations of apelin, fetuin-A, and procalcitonin were increased in subjects with acromegaly. There were significant correlations between apelin, fetuin-A, and procalcitonin in subjects with acromegaly. Carotid intima medial thickness values were similar between control subjects and subjects with acromegaly. Conclusions Carotid intima medial thickness was not increased in subjects with acromegaly. It is possible that the increased apelin and fetuin-A concentrations observed play a protective role against the development of atherosclerosis in subjects with acromegaly.

Adiponectin and Cardiac Hypertrophy in Acromegaly.

BACKGROUND Adiponectin is an adipocytes-derived hormone which has been shown to possess insulin-sensitizing, antiatherogenic, and anti-inflammatory properties. In acromegaly, the data on adiponectin is contradictory. The relationship between adiponectin levels and cardiac parameters has not been studied. OBJECTIVES The aim of this study was to find out how adiponectin levels were affected in acromegalic patients and the relationship between adiponectin levels and cardiac parameters. MATERIAL AND METHODS We included 30 subjects (15 male, 15 female), diagnosed with acromegaly and 30 healthy (10 male, 20 female) subjects. Serum glucose, insulin, GH, IGF-1 and adiponectin levels were obtained and the insulin resistance of the subjects was calculated. Echocardiographic studies of the subjects were performed. RESULTS We determined that adiponectin levels were significantly higher in the acromegalic group than the control group. In the acromegalic group, there was no statistically significant relation between serum adiponectin and growth hormone (GH), or insulin-like growth factor-1 (IGF-1) levels (p = 0.3, p = 0.1). We demonstrated that cardiac function and structure are affected by acromegaly. IVST, PWT, LVMI, E/A ratio, DT, ET, IVRT, VPR, and LVESV values were increased and the results were statistically significant. In the acromegalic group, adiponectin levels were positively related with left ventricle mass index (LVMI) but this correlation was found to be statistically weak (p = 0.03). In our study, there was a positive correlation between VAI and LVM. We also could not find any correlation between VAI and adiponectin levels. CONCLUSIONS Although insulin resistance and high insulin levels occur in active acromegaly patients, adiponectin levels were higher in our study as a consequence of GH lowering therapies. Our study showed that adiponectin levels may be an indicator of the cardiac involvement acromegaly. However, the usage of serum adiponectin levels in acromegalic patients as an indicator of cardiac involvement should be supported with other, wide, multi-centered studies.

Dehydroepiandrosterone sulfate levels in Turkish obese patients

PurposeObesity is well known to be linked to higher morbidity and mortality. Elevated plasma levels of free dehydroepiandrosterone (DHEA) are associated with reduced obesity and more limited accumulation of abdominal body fat. In contrast, the relationship between the DHEA sulfate ester (DHEAS) and adiposity is inconsistent and contradictory.MethodsThe aim of this study was to compare DHEAS levels in obese Turkish individuals, 37 men and 246 women. A variety of fatness, hormone, and blood parameters were measured.ResultsStatistically significant differences were found between male and female individuals with respect to weight, waist circumference, fat %, insulin, and DHEAS levels.ConclusionsWe found that in the Turkish population, while a correlation between obesity parameters and DHEAS levels exists in both female and male individuals, DHEAS levels are significantly higher in obese male individuals than in obese female individuals.

Resistin and Leptin Levels in Acromegaly: Lack of Correlation With Echocardiographic Findings

Purpose To find out how resistin and leptin levels were affected in patients with acromegaly and whether there is a relation between resistin levels and cardiac parameters. We also aimed to investigate whether resistin and leptin may be a link between insulin resistance and cardiac functions as well as these affected cardiac functions in the patients with acromegaly. Methods We included 30 subjects (15 men and 15 women) who had a diagnosis of acromegaly and 30 healthy (10 men and 20 women) subjects. Serum glucose, insulin, growth hormone, insulinlike growth factor 1 (IGF-1), resistin, and leptin levels were obtained, and insulin resistance of subjects were calculated. Echocardiographic studies of the subjects were performed. Results Resistin levels of the patients with acromegaly were found lower than controls. This difference was statistically significant (P = 0.001). Leptin levels were lower in the patients with acromegaly than in the controls, but this difference was not statistically significant. Resistin and leptin levels were not correlated with growth hormone, IGF-1, and with insulin-like growth factor binding protein 3 levels. Homeostasis model assessment of insulin resistance was positively correlated with resistin levels. (P = 0.03; r = 0.531) but not correlated with leptin levels. There was a positive correlation between body mass index and leptin levels in the patients with acromegaly (P = 0.007; r = 0.482). Interventricular septum thickness, posterior wall thickness, left ventricle mass index, peak early mitral inflow velocity–peak late mitral inflow velocity ratio, deceleration time, ejection time, isovolumetric relaxation time, velocity propagation, and left ventricular end-systolic volume values were significantly greater in the patients with acromegaly. Leptin levels in the acromegalic patients were not correlated with any of them. Conclusions We found biventricular hypertrophy and impairment of diastolic and systolic function in the patients with acromegaly. We conclude that changes in resistin and leptin levels are unlikely to account for the insulin resistance of acromegaly. They do not also seem to be contributing factors of cardiovascular changes in patients with acromegaly.