No abstract

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.

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. 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. In patients using only oral antidiabetic agents, after exchanging the treatment with insulin, on 3 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). 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.