Relationship Between Adipokines, Inflammation, and Vascular Reactivity in Lean Controls and Obese Subjects With Metabolic Syndrome

Abstract

PURPOSE: Metabolic syndrome is an important risk factor for cardiovascular disease. Adipokines interfere with insulin action and endothelial cell function. We investigated the relationship among adipokines, metabolic factors, inflammatory markers, and vascular reactivity in obese subjects with metabolic syndrome and lean controls. METHODS: Cross-sectional study of 19 obese subjects with metabolic syndrome and 8 lean volunteers evaluated as controls. Vascular reactivity was assessed by venous occlusion pletysmography measuring braquial forearm blood flow (FBF) and vascular resistance (VR) responses to intra-arterial infusions of endothelium-dependent (acetylcholine-Ach) and independent (sodium nitroprusside-SNP) vasodilators. Blood samples were obtained to evaluate C reactive protein (CRP), plasminogen activator inhibitor 1 (PAI-1), fibrinogen, adiponectin, resistin, and lipid profile. Patients were classified with regard to insulin resistance through the HOMA-IR index. RESULTS: PAI-1, CRP and fibrinogen were higher and adiponectin was lower in metabolic syndrome subjects compared to controls. Metabolic syndrome subjects had impaired vascular reactivity. Adiponectin and PAI-1 were associated with insulin, HOMA-IR, triglycerides, and HDLc; and resistin with CRP. Adiponectin was associated with VR after Ach in the pooled group and resistin with D FBF after Ach in the metabolic syndrome group. CONCLUSION: Metabolic syndrome subjects exhibited low levels of adiponectin and high levels of CRP, fibrinogen, and PAI-1. Adiponectin and PAI-1 correlated with insulin resistance markers. Adiponectin and resistin correlated with vascular reactivity parameters. An adipocyte-endothelium interaction might be an important mechanism of inflammation and vascular dysfunction.

Adiponectin as a tissue regenerating hormone: more than a metabolic function

“…fAd is also involved in the recruitment of progenitor endothelial cells (ePC) [82]. ePC recruitment is significantly reduced in type 2 diabetes mellitus (T2 DM), which is characterized by severe vascular disease mainly caused by the imbalance between endothelial injury and hampered endothelial repair [83]. Several studies report that T2 DM could affect the function of circulating ePC, by impairing migration [84,85], [15]; on mesoangioblasts by activating proliferation, cell motility, myogenesis, and inhibiting both apoptosis and anoikis [60]; on hemopoietic stem cells [71] and hippocampal neural stem cells by inducing cell proliferation [72].…”

Treatment of Obese Diabetic Mice With a Heme Oxygenase Inducer Reduces Visceral and Subcutaneous Adiposity, Increases Adiponectin Levels, and Improves Insulin Sensitivity and Glucose Tolerance

“…Excessive generation of reactive oxygen species (ROS) in diabetes is the underlying mechanism of endothelial injury, resulting in an accelerated rate of apoptosis and endothelial cell sloughing (3,4). In addition, reduced plasma adiponectin levels have been documented in patients with coronary artery disease and diabetes, presumably as a result of an increase in ROS (5,6).…”

Síndrome metabólico: Bases clínicas y fisiopatológicas para un enfoque terapéutico racional

“…También disminuiría la producción hepática de glucosa y la lipólisis. La disminución de adiponectina se asocia, en modelos experimentales y clínicos, con SM y progresión de enfermedad cardiovascular 31 .…”