Aim: Adipose tissue is now regarded as a source of proinflammatory mediators which may contribute to vascular injury, insulin resistance (IR), and atherogenesis, however, some of them have a protective role against vascular inflammation and/or IR; namely adiponectin and nitric oxide (NO). Adiponectin is a fat derived hormone, which enhances insulin sensitivity. In experimental studies adiponectin was shown to have anti-atherogenic properties by suppressing endothelial expression of adhesion molecules as endothelial-selectin (E-selectin) and inflammatory cytokines as high-sensitivity C-reactive protein (hsCRP), interleukin-1β (IL-1β), and monocyte chemotactic protein-1 (MCP-1). Therefore, the aim of the study was to evaluate plasma adiponectin, E-selectin, hsCRP, IL-1β, and MCP-1 concentrations in obese patients with and without coronary heart disease (CHD) having type 2 diabetes mellitus (DM) and evaluation of their relationship with selected anthropometric, biochemical, and clinical parameters.
Methods: The study group consisted of (N.=70) males, 20 of which served as healthy non-obese controls (group I) (mean age 38.5±3.7 years; mean BMI 28±1.2 kg/m2). Patients enrolled in the study were classified into the following groups: type 2 DM obese subjects without CHD (group II) (N.=25) (mean age 42.2±3 years; mean BMI 32.1±1.4 kg/m2) and type 2 DM obese subjects with CHD (group III) (N.=25) (mean age 40.6±3 years; mean BMI 31.5±1.2 kg/m2). Glucose and insulin estimation was performed and insulin resistance index (HOMA-IR) was calculated. In the fasting state, the plasma HbA1c, adiponectin, E-selectin, in comparison to hsCRP, IL-1β, MCP-1, and lipid parameters were estimated.
Results: FBG, HbA 1c %, lipids, insulin, MDA, NO, hsCRP, IL-?, MCP-1, Adiponectin as well as E-selectin concentration were significantly different in patients with type 2 DM and CHD in comparison to patients without CHD and moreover, the healthy control group (P=0.01). There was a significant negative correlation between adiponectin and E-selectin (r=-0.642; P=0.0001).
Conclusion: Our study supports the hypothesis that decreased level of adipokine(s), together with increased oxidative stress, pro-inflammatory marker(s) as well as endothelial adhesion molecule(s) contributes to the complex process of atherosclerosis in type 2 diabetic obese patients that may lead eventually to CHD.