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

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.

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.

Choice of treatment based on Turkish hypertension consensus report: Do we follow the recommendations?

OBJECTIVE: The aim of this study was to determine how often the recommendations of the Turkish Hypertension Consensus Report are followed, and to draw attention to the report. METHODS: The demographic information of 1000 patients diagnosed with hypertension and the details of the antihypertensive medications prescribed at the outpatient service of a tertiary care hospital were recorded, and the data were compared with the recommendations of the report. RESULTS: The mean age of the patients was 62±11 years. In all, 623 (62.3%) of the 1000 patients were women, and 377 (37.7%) were men. A combination of an angiotensin II receptor blocker (ARB) and a diuretic was the most frequently observed prescription. A diuretic was the most used antihypertensive drug (58.7%), followed by an ARB (48.8%). However, as a monotherapy, a calcium channel blocker (CCB) was the most commonly used antihypertensive drug (19.2%). The most frequently used antihypertensive drug group in older patients was diuretics (63.6%), as proposed in the report. Beta blockers (49.1%) were used more often than expected. For the diabetic group also, a diuretic (60.7%) was the most frequently used antihypertensive drug, followed by an ARB (51.1%) and a CCB (45.2%). Angiotensin-converting enzyme (ACE) inhibitors (34.6%) were the fifth most preferred antihypertensive drug class. However, when ACE inhibitors and ARBs were considered as a single group, known as renin-angiotensin system (RAS) blockers, these RAS blockers were the most prescribed antihypertensive drug class, followed by diuretics. In the group of patients with coronary artery disease, treatment was found to be generally consistent with the report, but the use of diuretics was greater than expected. Lastly, 124 of 160 patients who had chronic kidney disease were given RAS blocker therapy, which was in line with the consensus report recommendations. CONCLUSION: Antihypertensive therapies were individualized, as suggested by the consensus report. However, there are proposals still to be considered in special patient groups.

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.

Effect of Glycemic Regulation on Endocan Levels in Patients With Diabetes: A Preliminary Study.

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.

Serum Endocan Level and the Severity of Coronary Artery Disease: A Pilot Study.

Endothelial-specific molecule 1 (endocan) is expressed in endothelial cells. We investigated the relationship between acute coronary syndrome (ACS) and serum endocan levels. We included 30 individuals as a control group and 53 patients diagnosed with ACS. The severity of coronary artery disease was assessed by a modified Gensini stenosis and SYNTAX scoring system. There was a significant difference in serum endocan levels between the control group and the ACS group (0.75 ± 0.13 vs 0.86 ± 0.25 ng/mL, P = .014). There was also a significant difference in serum endocan levels between diabetic patients with ACS and nondiabetic patients with ACS (1.02 ± 0.33 vs 0.81 ± 0.21 ng/mL, P = .016). There was no significant correlation between serum endocan level, Gensini, and SYNTAX score (r = .11, P = .53 and r = .16, P = .37). Endocan, a new biomarker of endothelial pathology, is significantly increased in patients with ACS.

Relationship between brain natriuretic peptide, microalbuminuria, and contrast-induced nephropathy in patients with acute coronary syndrome.

OBJECTIVE: Patients may develop kidney failure because of the contrast agent given during coronary angiography. Renal dysfunction and heart failure were previously shown to be associated with the development of contrast nephropathy. In our study, we aimed to investigate whether there is a relationship between subclinical renal (indicated by microalbuminuria) and/or cardiac (indicated by the height of the BNP) dysfunction between the development of contrast-induced nephropathy on patients undergoing angiography due to acute coronary syndrome. METHODS: This is an observational prospective cohort study. A total of 170 patients hospitalized with a diagnosis of acute coronary syndrome in the coronary care unit were included in this study. Blood samples were collected from 145 patients without microalbuminuria and 25 patients with microalbuminuria to determine their BNP levels before coronary angiography. The patients' urea and creatinine levels were examined before and 72 h after coronary angiography. Statistical analysis was performed using Kolmogorov-Smirnov test, Mann-Whitney U test, independent samples t-test and the chi-square test. RESULTS: The study subjects included 82 females and 88 males (average age, 64.4±14.5 years). The BNP levels and height distribution of the 145 patients without microalbuminuria were compared between those with and without contrast agent-induced nephropathy, but no significant difference was found (205.6±280.6, 198.0±310.0, p=0.817). Similarly, no relationship between the microalbumin level and contrast agent-induced nephropathy was found in 25 patients. CONCLUSION: A relationship between BNP, microalbuminuria, and contrast agent-induced nephropathy was not found in patients hospitalized in a coronary care unit with a diagnosis of acute coronary syndrome who were scheduled for coronary angiography. Additional multicenter studies with larger patient groups should be conducted to obtain more data.