Dysregulation of omentin, a beneficial adipokine, and apelin, an inflammatory adipokine, is thought to play a role in the development of type 2 diabetes mellitus and cardiovascular disease. The objective of this study was to evaluate the relationship between circulating omentin and apelin concentrations and components of the metabolic syndrome in adults with and without type 2 diabetes mellitus or cardiovascular disease. A total of 240 adults, sex-and age-matched, were included in the current case-control study, including 80 healthy, non-obese controls, 80 obese patients with T2DM without cardiovascular disease, and 80 obese patients with T2DM with cardiovascular disease. A fasting blood sample was collected to determine biochemical indicators and insulin resistance index (HOMA-IR). Omentin, apelin, interleukin-1β (IL-1β), troponin-T, and oxidized LDL (Ox-LDL) plasma level was assessed by ELISA. Associations of adipokines with biochemical parameters of the patients were determined. Serum omentin levels were significantly lower and serum apelin and IL-1β concentrations were significantly higher in obese diabetic groups compared to non-obese controls. In correlation analyses, omentin negatively associated with the HOMA-IR index, apelin, and troponin-T, whereas apelin was positively associated with IL-1β, BMI, and troponin-T. Our study supports the hypothesis that abnormal production of omentin and apelin can contribute to the pathogenesis of obesity-related complications including T2DM and cardiovascular disease.

Background and aim: Dysregulation of omentin, a beneficial adipokine and apelin, an inflammatory adipokine, is thought to play a role in the development of type 2 diabetes mellitus and cardiovascular disease. The objective of this study was to evaluate the relationship between circulating omentin and apelin concentrations and components of the metabolic syndrome in adults with and without type 2 diabetes mellitus or cardiovascular disease. Methods: A total of 240 adults sex and age-matched were included in the current case-control study, including 80 healthy non-obese controls, 80 obese patients with T2DM without cardiovascular disease, and 80 obese patients with T2DM with cardiovascular disease. Fasting blood sample was collected to determine biochemical indicators and insulin resistance index (HOMA-IR). Omentin, apelin, interleukin-1β (IL-1β), troponin-T, and oxidized LDL (Ox-LDL) plasma level was assessed by ELISA. Associations of adipokines with biochemical parameters of the patients were determined. Results: Serum omentin levels were significantly lower and serum apelin and IL-1β concentrations were significantly higher in obese diabetic groups compared to non-obese controls. In correlation analyses, omentin negatively associated with the HOMA-IR index, apelin, and troponin-T, whereas apelin was positively associated with IL-1β, BMI, and troponin. Conclusions: Our study supports the hypothesis that abnormal production of omentin and apelin can contribute to the pathogenesis of obesity-related complications including T2DM and cardiovascular disease.

Type 2 diabetes mellitus (T2DM) is a metabolic pro-inflammatory disorder characterized by chronic hyperglycemia and increased levels of circulating cytokines. Adiponectin, tumor necrosis factor-α (TNF-α), interleukin-6 (Il-6), are important cytokines mediators in the pathogenesis of T2DM. The single nucleotide polymorphisms (SNPs) present in the regulatory regions of cytokine genes often have an impact on their expression levels.Aim: Explore potential associations between SNP+276 G/T of adiponectin, SNP -308 G/A of TNF-α and SNP -174 C/G of IL-6 genes with T2DM and to assess its influence on their serum levels. Subjects and Methods:From the Egyptian population, we enrolled 95 T2DM patients and 85 non-diabetic controls. Serum adiponectin, TNF-α and IL-6 were measured. Genotyping for three SNPs of the adiponectin, TNF-α and IL-6 genes was performed by polymerase chain reaction-restriction fragment length polymorphism.Results: Subjects with the GT/TT genotype of SNP 276 were at increased risk for T2DM (OR=15.88, CI=7.56-33.31, P ≤ 0.01) and associated with hypoadiponectinemia compared with the GG genotype. Furthermore, the allelic frequency of the A allele of SNP 308 was significantly different between T2DM patients compared to controls (X 2 =30.54, P ≤ 0.0001). Moreover, Individuals with T2DM carrying the GA/AA genotypes had significantly higher serum TNF-α levels than those carrying GG genotype. In addition, Carriers of G allele of IL-6 were significantly more likely associated with T2DM.

Background and aim: The goal of this study was to evaluate the role of serum Omentin andapelinin obese patients having type 2 diabetes mellitus with and without cardiovascular disease compared to the healthy control group and evaluation of their association with selected anthropometric, biochemical, and clinical parameters. Methods:A total of 240 adults sex and age-matched were included in the current case--control study. 80 of which served as healthy non-obese controls. Patients enrolled in the study were classified into the following groups: 80 type 2 diabetic obese subjects without cardiovascular disease and 80type 2 diabetic obese subjects with cardiovascular disease. Fasting blood sample was collected to determine biochemical indicators and insulin resistance index (HOMA-IR). Omentin, apelin, interleukin-1β (IL-1β), troponin-T, and oxidized LDL (Ox-LDL) plasma level was assessed by ELISA. Association of adipokines with biochemical markers was studied.Results: Levels of Omentin were lower in obese diabetic groups than non-obese controls. On the other hand apelin and IL-1β levels showed higher significant values in obese diabetic groups compared to healthy ones. In correlation analysis, Omentin was negatively associated with insulin resistance index, apelin, and troponin-T. On the other hand, apelin was positively associated withIL-1β, BMI, and troponin-T. Conclusion:Our study supports the hypothesis that deregulated production of adipokines; Omentin and apelin owing to adipose tissue dysfunction can contribute to the pathogenesis of obesity-linked complications that may lead eventually to type 2 diabetes mellitus and cardiovascular disease.