Endothelial-specific molecule 1 (endocan) is expressed by endothelial cells and may have a major role in the regulation of cell adhesion and in the pathogenesis of inflammatory disorders. We aimed to assess change in endocan levels after 3 months of lifestyle change recommendations and guideline-based treatment. Diabetic patients (n = 77) who had neither chronic kidney disease nor chronic inflammatory disease were included. After baseline evaluation, the patients were advised lifestyle changes, and their medical treatment was determined individually according to recommendations of the American Diabetes Association (ADA) guidelines. At the end of third month patients were reevaluated. Baseline endocan levels were significantly increased in the study group compared with the control group. The third-month laboratory workup showed significant reductions in hemoglobin A1c, urinary albumin-to-creatinine ratio (UACR), and endocan levels. Only δ-UACR was independently correlated with δ-endocan in multivariate linear regression analysis. Our findings suggest that serum endocan concentrations are elevated in patients with type 2 diabetes and decrease following anti-hyperglycemic treatment. Furthermore, decrease in endocan concentrations might be associated with improved glycemic control and reductions in UACR.

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Objectives: Adropin is a novel marker of metabolic syndrome and insulin resistance. The aim of this study was to explore the association of serum adropin levels with hepatosteatosis among adult patients. Materials and Methods: Serum biochemical parameters including liver and renal function tests, insulin levels, and serum adropin levels were compared between adult patients with nonalcoholic fatty liver disease (NAFLD) and healthy control cases. Results: A total of 51 patients with a mean age of 37.9 ± 9.96 years diagnosed with grade 2–3 hepatosteatosis and 30 healthy control cases with a mean age of 34.8 ± 9.5 years were included in the study. Serum adropin levels in the NAFLD group were statistically significantly lower than in the control cases (588.4 ± 261.0 vs. 894.2 ± 301.2, respectively; p < 0.001). The study participants were further subdivided into 2 groups as patients with (n = 35) or without (n = 46) insulin resistance using the serum homeostatic model of assessment-insulin resistance (HOMA-IR). Serum adropin levels were statistically significantly lower in patients with insulin resistance (p < 0.01). There was a negative correlation between adropin levels and serum insulin, HOMA-IR, urea, gamma-glutamyl transferase, total cholesterol, and triglyceride levels. Conclusion: We observed a decrease in serum adropin levels among adult patients with NAFLD. We also found lower levels of serum adropin in patients with insulin resistance, supporting previous data in the literature. Studies investigating the association of adropin levels with other inflammatory parameters are warranted to define its exact role in the pathogenesis of hepatosteatosis.

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Background and ObjectivesSubclinical hypothyroidism (SH) is considered to be a potential risk factor for cardiovascular disease. Epicardial adipose tissue (EAT) thickness is also closely related to cardiovascular disorders. The aim of this study was to evaluate whether SH is associated with higher EAT thickness.Subjects and MethodsFifty-one consecutive patients with SH and 51 healthy control subjects were prospectively enrolled into this trial. Thyroid hormone levels, lipid parameters, body mass index, waist and neck circumference, and EAT thickness measured by echocardiography were recorded in all subjects.ResultsMean EAT thickness was increased in the SH group compared to the control group (6.7±1.4 mm vs. 4.7±1.2 mm, p<0.001). EAT thickness was shown to be correlated with thyroid stimulating hormone level (r=0.303, p=0.002). Multivariate logistic regression analysis revealed that EAT thickness was independently associated with SH {odds ratio (OR): 3.87, 95% confidence interval (CI): 1.92-7.78, p<0.001; OR: 3.80, 95% CI: 2.18-6.62, p<0.001}.ConclusionEpicardial adipose tissue thickness is increased in patients with SH compared to control subjects, and this increase in EAT thickness may be associated with the potential cardiovascular adverse effects of SH.

Antihypertensive therapies were individualized, as suggested by the consensus report. However, there are proposals still to be considered in special patient groups.

Objective: Activated macrophages (M1-type macrophages) in adipose tissue secrete many proinflammatory cytokines that induce insulin resistance (IR). Oncostatin M (OSM), a member of the interleukin-6 (IL-6) family of Gp130 cytokines, plays an important role in a variety of biological functions, including the regulation of inflammatory responses. Proinflammatory cytokines released in patients with IR trigger a chronic, low-grade inflammatory reaction in blood vessel walls. This inflammator response leads to endothelial damage, which is the main mechanism for atherosclerosis and many cardiovascular diseases. Animal studies have reported a relationship between OSM and IR. To the best of our knowledge, however, few clinical studies have examined this topic. Therefore, we studied the relationship between serum levels of OSM and IR. Subjects and methods: This prospective cross-sectional case-control study enrolled 50 people with IR (according to the HOMA-IR and QUICKI indices) and 34 healthy controls. The fasting blood concentrations of insulin, glucose, blood urea nitrogen (BUN), creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglyceride, total cholesterol, C-reactive protein (CRP), and OSM were determined. Results: There were no significant differences between the two groups in age, sex, and HbA1c levels. Univariate analyses showed that waist circumference (WC) and levels of fasting glucose, insulin, CRP, HDL-C, OSM, HOMA-IR, and QUICKI differed between the two study groups. In multivariate analyses, both IR indices (QUICKI and HOMA) and OSM differed between the two groups. Conclusion: OSM was correlated with the IR indices (QUICKI and HOMA). For simplicity, it might replace the other IR indices in the future. Further detailed studies are needed to confirm this.

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