ACTA ENDOCRINOLOGICA (BUC)

Introduction. Purslane (Portulaca oleracea L.) has antioxidant effects. The aim of this study was to evaluate the pancreas protective effect of Purslane hydroalcoholic extract in D-galactose induced aging female mouse model. Methods. In this experimental study, 72 adult female mice (30 – 35 g) were obtained and divided into 6 groups: control, Purslane hydroalcoholic extract, D-galactose, D-galactose + Purslane hydroalcoholic extract, Aging, Aging + Purslane hydroalcoholic extract. The aging model induced by subcutaneous injection of D-galactose for 45 consecutive days, and Purslane hydroalcoholic extract was orally gavaged in the last 21 days. 24 hours after the last drug and extract administrations, serum samples and pancreas tissues were removed for biochemical and histological assessments. Results. Glucose decreased in the Purslane, D-galactose + Purslane and Aging + Purslane groups (p<0.05). Insulin and HOMA-IR increased in D-galactose and, Aging groups (p<0.05). Furthermore, administration of hydroalcoholic extract of Purslane improved these parameters in D-galactose and Aging treated mice (p<0.05). Diameter of pancreatic islets decreased in Aging and D-galactose groups and Purslane hydroalcoholic extract administration improved this variable. Conclusions. The present results show that Purslane has pancreas protective effects via its hypoglycemic and insulin resistance reducing activity.

Aim. We investigated the relationship between irisin concentrations and glycemic control, body composition and anthropometric measures in children with type 1 diabetes mellitus. Methods. The study involved 40 subjects with T1DM prospectively. Glycemic control was evaluated. Body composition was analyzed with a bioimpedance analyzer (BIA). Serum irisin concentrations were measured using an ELISA kit. Results. Irisin levels were found higher in BMI <17 kg/m2 group (p=0.002) compared to BMI >17 kg/m2. Irisin level was negatively correlated with weight, height, BMI, fat free mass, skeletelal muscle mass, basal metabolic rate (r= -0.40, p= 0.011; r=-0.32, p=0.046; r=-0.366, p= 0.022; r=-0.423, p= 0.007; r=-0.430, p=0.006; r=-0.416, p=0.009, respectively); there was a strong correlation between LDL-C and irisin levels (r=0.367, p=0.02). In multivariate linear regression analyses model, irisin concentrations were correlated with weight (ß-coefficient= - 0.391, p= 0.015). LDL-C is associated, but not correlated significantly with irisin levels, (ß-coefficient =0.272, p=0.084). Conclusion. As a result, weight and LDL-C were the predictors of circulating irisin. To our knowledge, this study is the first examining association between irisin levels and body composition comprehensively, in children with type 1 diabetes mellitus.

Objective. We aimed to investigate whether lifestyle and body fat mass have an impact on the occurence of nonfunctional adrenal incidentalomas (NFAI). Methods. 100 patients with NFAI were included . 50 people constituted the control group. Physical activities of these groups were evaluated (using the International Physical Activity Questionnaire), smoking status was determined, anthropometric measurements were made. Body fat mass, fat percentage, total body water and fat free mass were measured using bioelectrical impedance method. Results. Body mass index (BMI), waist, hip, neck circumference, total body fat percentage and fat mass and smoking rate were found to be statistically higher in the patient group. Physical activities did not differ significantly. When a subgroup with similar age and BMI among was created, waist circumference and total fat mass were again significantly higher in the patient group. There was a significant positive correlation between the size of the adrenal mass and waist, neck circumference, BMI, and cortisol after 1 mg dexamethasone suppression test. Conclusion. The increase in the fat mass may have an impact on the development of NFAI. Although the patients were regarded as nonfunctional, suppressibility of the cortisol decreases as the mass size of the incidentaloma increases.

Objective. In this study we investigated the effect of dorsomedial hypothalamus (DMH) neuropeptide Y (NPY) knock-down on hepatic insulin sensitivity in high-fat (HF) diet-fed rats. Methods. Forty-eight Sprague-Dawley rats were randomly assigned to receive bilateral DMH injections of adeno-associated virus AAVshNPY or AAVshCTL and then accessed to regular chow. Five weeks after viral injection, half rats in each group were given access to the HF diet. At 16 weeks, rat livers were collected. Insulin receptor substrate-1 (IRS-1) and phosphoinositide 3-kinase (PI3K) mRNA expression was measured by qRT-PCR. Blood glucose levels were measured by the oxidase method, serum insulin, triglyceride, and TC levels were measured by Elisa. Pathological changes in the liver were assessed by hematoxylin-eosin (HE) staining. AKT, p-AKT, and GSK-3 levels were measured by western blotting. Results. Compared with AAVshCTL-injected rats, AAVshNPY-injected rats showed a significant decrease in blood glucose concentrations; serum insulin, triglyceride, and TC; HOMA-IR; and IRS-1 and PI3K mRNA levels (P<0.05). ISI, GSK-3, and p-AKT levels were significantly increased (P<0.05). HE staining showed that AAVshNPYinjected rats fed the HF diet had mild fatty degeneration. Conclusion. These results suggest that DMH NPY knock-down improves hepatic insulin sensitivity in HF diet-fed rats by activating the hepatic PI3K/AKT insulin signalling pathway.

Context. Abnormally increased hepatic glucose production contributes to hyperglycemia in diabetes. Interventions that suppress hepatic gluconeogenesis should be beneficial in improving glycemic control in patients with diabetes. Objectives. It has been suggested that hepatic FTO is involved in glycemic control by regulating gluconeogenesis. Both FTO and activating transcription factor 4 (ATF4) positively regulate the expression of gluconeogenic genes in the liver, suggesting the possibility that ATF4 mediates the stimulatory effect of FTO on hepatic gluconeogenesis. The present study aimed to determine the effect of altered expression or activity of FTO on Atf4 and gluconeogenic gene expression in hepatocyte cells. Methods. Mouse hepatocyte AML12 cells were treated with the FTO inhibitor rhein or transfected with an FTO-expressing plasmid. Levels of gluconeogenic glucose- 6-phosphatase (G6pc) and Atf4 mRNA and protein were measured. Results. Rhein treatment significantly reduced G6pc mRNA levels as well as Atf4 mRNA and protein levels. Conversely, enhanced FTO expression caused an increase in G6pc and Atf4 mRNA levels. Conclusions. These findings support the hypothesis that hepatic FTO participates in the regulation of hepatic gluconeogenic gene and ATF4 expression. Reducing the activity of the hepatic FTO-ATF4 pathway may be beneficial in reducing hepatic glucose production and ameliorating hyperglycemia in diabetes.

Context. With more studies investigating effects of high serum lipid levels, new findings are emerging regarding the damage these biomolecules may cause. Aim. In this study we aimed to find a relation between neuropathy and hypertriglyceridemia in patients with metabolic syndrome (MS). Material and methods. One hundred and twenty subjects (Ninety subjects with metabolic syndrome and 30 healthy controls) were included in the study. Subjects with MS were divided into three groups. HbA1C levels of the subjects were < 5.7% in group A, ≥ 5.7% - < 6.5% in group B, and ≥ 6.5% - < 8.0% in group C. Pin-Prick test and Semmes- Weinstein Monofilament were used for neurological examination. Electromyography was performed to patients with neuropathy to support the diagnosis. Results. Neuropathy prevalence was found to be higher in the subjects with metabolic syndrome compared to control group. (9.9 %; 16.65 %; 23.31 % vs. 3.3%; in group A, group B, group C vs. healthy control group respectively) (p=0.003 for group A, p=0.0002 for group B, p=0.0002 for group C). There was an association between triglyceride levels and neuropathy in group C. Conclusion. Patients with MS may have more neuropathy risk than we estimate.

Polycystic ovary is a common cause of infertility due to anovulation. Objective. The aim of this study was to improve maturation of oocyte in cultures of follicles derived from mouse polycystic ovary by hydrostatic pressure. Subjects and Methods. Female NMRI mice 12-14 days old were injected daily with testosterone enanthate 1 mg/100g body weight dissolved in sesame oil (PCO group), for inducing polycystic ovary (PCO) while non-PCO group were injected only with vehicle for 2 and 4 weeks. The ovaries were fixed and then were used for histological studies. The isolated preantral follicles were cultured for 12 days. Follicles with good quality have been induced using human chorionic gonadotropin (HCG) for in vitro maturation. Then follicles from each group either were transferred to pressure chamber and subjected to 20 mmHg pressure for 30 min or no treated by hydrostatic pressure. Follicles from two groups were cultured for 24 and 48 h and the in vitro maturation of oocytes was assessed. Results. Testosterone enanthate treatment causes the histological changes in mouse ovary and significantly increased the percentage of cystic follicles and decreased the percentage of preantral and antral follicles in PCO group, in comparison to non-PCO group after four-week treatment) (P<0.05). (The in vitro maturation rate in hydrostatic pressure treated follicles was higher than in those not treated by hydrostatic pressure (P < 0.05). Conclusions. This study demonstrated that hydrostatic pressure can improve maturation of oocyte in cultures of follicles derived from mouse polycystic ovary.

Introduction. Thyroid diseases may cause endothelial dysfunction. Asymmetric dimethylarginine (ADMA) levels in patients with thyroid dysfunction were analyzed by few studies.\r\nAim.We aimed to compare ADMA levels in patients with hyperthyroidism in a cohort free of cardiovascular risk associates such as diabetes or chronic renal failure with further comparison with healthy control subjects.\r\nMaterials and methods. The study took place in Duzce University Medical Faculty, Cardiology and Internal Medicine\r\nDepartment during the year 2010. The study group consisted of patients with hyperthyroidism (overt and subclinical). The patients with renal failure, diabetes and severe\r\nhypertension were excluded.\r\nResults. Mean ADMA level was 1.04 ? 0.43 &#956;mol/L in the hyperthyroid group and 0.68 ? 0.21 &#956;mol/L in the control group (p&#8804;0.001). The comparison of patients with hyperthyroidism according to the etiology (three groups as Graves?, multinodular goiter and thyroiditis) did not show any significant difference.\r\nConclusion. Asymmetric dimethylarginine increases in patients with hyperthyroidism regardless of the etiology.\r\nThe increase of ADMA levels is independent of known major cardiovascular risk factors. It may reflect the possible counteraction of endothelial dysfunction in the pathogenesis of atherosclerosis in hyperthyroidism beyond the known cardiovascular risk factors.

Aim. To assess the levels of s BGP and BAP and correlate them with the rate of bone remodelling.\r\nPatients and Methods. The study was performed on 74 cases with postmenopausal osteoporosis, divided into two groups, according to the duration of estrogenic deprivation, compared with a control group (n= 20, postmenopausal women without osteoporosis). The serum levels of the discussed markers were measured by ELISA technique. BMD was measured using the DXA technique with the assessment of T score.\r\nResults. In the group I: BGP were 20.12?0.87ng/mL (p<0.03), those of BAP 13.76?0.6&#956;g/mL (p<0.001) and sT spine were -3.63?0.65DS (p<0.001). In the group II: BGP were 15.12?1.55ng/mL (p<0.05), those of BAP 11.88?0.38&#956;g/mL (p<0.001) and sT spine were -3.78?0.36DS (p<0.001). The control group presented: BGP of 16.22?1.62ng/mL, those of BAP of 8.68?0.44&#956;g/mL and sT spine of -1.78?0.11DS. The serum levels of BGP in postmenopausal osteoporosis cases were increased in group I (suggesting an osteoblastic activation) and decreased in group II (probably secondary to the stimulation of osteoblastic apoptosis). The serum levels of BAP are significantly increased\r\nin postmenopausal osteoporosis versus control group, attesting osteoblastic activation.\r\nConclusion. Bone resorption begins gradually to outrun a new bone formation rhythm associated with low BMD.

Background. sRANKL (soluble receptor activator of nuclear factor-kB ligand) and OPG (osteoprotegerin) represent a novel cytokine system with pleiotropic effects on bone remodeling.\r\nAim. The aim of this study was to assess the implications of serum levels of sRANKL, OPG and E2 (estradiol) in the process of bone remodeling of postmenopausal women with osteoporosis.\r\nMethods. The study was performed on 74 patients with postmenopausal osteoporosis, divided into two groups of patients according to the duration of estrogenic deprivation, compared with a control group (n= 20 postmenopausal women without osteoporosis). The serum levels of the enunciated markers were measured by ELISA technique.\r\nResults. In the group I (n= 48, bellow 15 yrs of estrogenic deprivation) the serum levels of sRANKL were 67.63?3.55 pg/mL (p<0.002), those of OPG were 42.15?0.55 pg/mL (p<0.002) and the levels of E2 were 28.32?1.78 pg/mL (p<0.004). In the group II (n= 26, over 15 yrs of estrogenic deprivation) the serum levels of sRANKL were 49.26?2.85 pg/mL (p<0.003), those of OPG 27.78?1.04 pg/mL (p<0.003) and the serum levels of E2 were 19.66?1.23 pg/mL (p<0.002). In the control group (n=20), the serum levels of sRANKL were 32.48?3.03 pg/mL, those of OPG 38.05?4.89 pg/mL and the serum levels of E2 were 43.07?4.04 pg/mL.\r\nConclusions. The serum levels of sRANKL are significantly higher in postmenopausal women with osteoporosis versus postmenopausal women without osteoporosis, attesting osteoclasts activation. The serum levels of OPG in postmenopausal women with osteoporosis were increased in group I, suggesting the osteoblastic activation and decreased in group II, probably secondary to the stimulation of osteoblastic apoptosis.