Association of serum adiponectin levels with artherosclerosis and the metabolic syndrome in obese children.

BACKGROUND: The atherosclerotic process starts at an early age and is linked to obesity. However, the exact pathophysiological mechanism is poorly understood. OBJECTIVE: To investigate the relationship between serum adiponectin and metabolic syndrome and early arteriosclerosis. SUBJECTS: 176 obese and 88 normal children. METHODS: Ultrasound measurement was performed to investigate IMT, FMD, carotid artery compliance (CAC). Adiponectin was measured by enzyme-linked immunosorbent assay. RESULTS: Adiponectin levels correlated negatively with obese markers, blood pressure, fasting insulin, high sensitive CRP, HOMA-IR and IMT; marginally positively associated with CAC and HDL-c. The risk of metabolic syndrome increased 3.43 times when adiponectin levels were less than 7060 ng/ml. Heavy obesity, hypertension, low HDL-c, fasting hyperinsulin, High LDL-c and metabolic syndrome percentage were different in three groups according to the cut-off value of adiponectin. CONCLUSIONS: Low adiponectin levels are associated with a high incidence of metabolic syndrome.

Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide.

AIM: To investigate the protective effects of prostaglandin E(1) (PGE(1)) against H(2)O(2)-induced oxidative damage on human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were pretreated with PGE(1) (0.25, 0.50, and 1.00 micromol/L) for 24 h and exposed to H(2)O(2) (200 micromol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. RESULTS: PGE(1) (0.25-1.00 micromol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H(2)O(2). PGE(1) also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE(1) significantly increased NO content, eNOS protein, and mRNA expression. CONCLUSION: PGE(1) effectively protected endothelial cells against oxidative stress induced by H(2)O(2), an activity that might depend on the up-regulation of NO expression.