Relationships among oncostatin M, insulin resistance, and chronic inflammation: a pilot study.

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.

Serum Angiopoietin-like peptide 4 levels in patients with hepatic steatosis.

OBJECTIVES: Angiopoietin-like peptide 4 (ANGPTL-4) plays an important role in lipid metabolism by inhibiting the enzyme lipoprotein lipase. This effect of ANGPTL-4 results in suppression of the release of plasma triglyceride-derived fatty acids. Increase in fatty acid levels entering to the liver and abnormalities in their secretion is one of the main mechanisms in pathogenesis of hepatic steatosis. In this study, we aimed to investigate the role of ANGPTL-4 in pathogenesis of hepatic steatosis by determining its levels in patients with fatty liver disease. METHODS: Totally 51 patients (age: 37.9 ±â€¯9.9 years, M/F) diagnosed with grade 2-3 hepatic steatosis with ultrasound and 30 healthy volunteers (age: 34.8 ±â€¯9.5 years, M/F) were included in the study. In both groups, routine biochemical tests including fasting blood glucose, fasting insulin levels, triglyceride, total cholesterol, LDL- cholesterol, HDL-cholesterol, AST, ALT, ALP, GGT levels were measured together with the ANGPTL-4 levels. In determination of ANGPTL-4 levels, ELISA was performed. RESULTS: When compared with the control group, ANGPTL-4 levels were determined to be decreased in patients with hepatic steatosis (369 ±â€¯243 vs 303 ±â€¯286 ng/mL, p = 0.014). There was a negative weak correlation observed between ANGPTL-4 and triglyceride levels (r = -0.246, p = 0.027). Among all groups, when patients with and without insulin resistance were compared; ANGPTL-4 levels were determined to be similar. While fasting blood glucose levels were similar between 2 groups; fasting insulin and triglyceride levels were determined to be increased in hepatic steatosis group (Insulin 17.7 ±â€¯12 vs 7.4 ±â€¯3.3 µIU/mL, p < 0.001, triglyceride 158 ±â€¯46.4 vs 118 ±â€¯59.8 mg/dL p < 0.001). CONCLUSIONS: We have determined lower serum ANGPTL-4 levels in patients with hepatic steatosis. ANGPTL-4 that is regulating LPL activity plays an important role in fatty liver disease pathogenesis via free fatty acid metabolism and peroxisome proliferator-activated receptor-delta (PPAR-δ). We believe that the results of this study would elucidate the investigations about the mechanism of fatty liver disease development and treatments targeting ANGPTL-4.

The Effects of Blood Glucose Regulation in Omentin-1 Levels among Diabetic Patients.

Objectives: Omentin-1, an adipocytokine that increases the insulin sensitivity, has been determined to be reduced in patients with insulin resistance, impaired glucose tolerance, and Type-2 diabetes mellitus. In this study, we have investigated the alterations in Omentin-1 levels with the blood glucose regulation in diabetic patients having poor glycemic control. By this way, we aimed to determine the role of Omentin-1 as a marker in follow-up and monitoring progression of diabetes. Methods: Totally 58 patients with type 2 diabetes mellitus, older than 18 years of age who were having poor glycemic control (HbA1c≥9) were included in this study. In the first visit, all clinical and biochemical parameters of patients were recorded. After baseline evaluation, the patients were advised life style changes, and their medical treatment was determined individually according to the recommendations of the American Diabetes Association guidelines. At the end of the third month patients were re-evaluated. Serum Omentin-1 levels were measured with ELISA. Results: In patients using only oral antidiabetic agents, after exchanging the treatment with insulin, on 3rd month of treatment, there was a significant decrease in serum C-peptide and Omentin-1 levels compared with the initial results (p=0.034, p=0.048, respectively). On the other hand, in patients using insulin treatment from the beginning of the study, there was not any significant alterations in serum C-peptide or Omentin-1 levels compared with the initial results (p>0.05). Conclusions: Serum Omentin-1 levels may change with insulin and metformin treatments in Type-2 diabetic patients. In patients with poor glycemic control, Omentin-1 levels do not change with the regulation of blood glucose levels. A decrease in Omentin-1 and C-peptide levels has been determined after the initiation of insulin therapy. This suggests that, Omentin-1 levels are closely associated with the endogenous insulin reserve and may be used in follow-up of patients.