title: Weight loss is associated with improved endothelial dysfunction via NOX2-generated oxidative stress down-regulation in patients with the metabolic syndrome.
abstract: The aim of this study was to assess whether adherence to a restricted-calorie, Mediterranean-type diet improves endothelial dysfunction and markers of oxidative stress in patients with metabolic syndrome. A moderately low-calorie (600 calories/day negative energy balance), low-fat, high-carbohydrate diet (<30% energy from fat, <10% from saturated fat and 55% from carbohydrate) was prescribed to 53 outpatients with the metabolic syndrome. Participants were divided into two groups according to body weight loss > or < 5% after 6 months. Group A (n = 23) showed a remarkable decrease in body weight (-6.8%), body-mass-index (-4.6%), waist circumference (-4.8%), HOMA-IR (-27.2%), plasma glucose, glycosylated haemoglobin, total and LDL-cholesterol, blood pressure, serum NOX2 (the catalytic core of NADPH oxidase) (-22.2%) and urinary8-isoprostanes (-39.0%) and an increase of serum NOx (Nitrite/Nitrate) (+116.8%) and adiponectine (+125.5%) as compared with those in group B (n = 30). A statistically significant increase in brachial artery flow-mediated dilatation was observed in group A (+24.7%; p < 0.001), while no changes were present in group B. Variations of flow-mediated dilatation were statistically and negatively correlated with changes of serum NOX2 levels (p = 0.04), body-mass-index (p < 0.01), waist circumference (0.01), glycosylated haemoglobin (p < 0.01), LDL-cholesterol (p < 0.01) and triglycerides (p < 0.05) and positively correlated with changes of serum NOx (p < 0.001) and adiponectin (p = 0.01). The results show that moderate weight loss is able to improve endothelial dysfunction in patients with the metabolic syndrome. The coexistent decrease of NOX2 activation suggests a role for oxidative stress in eliciting artery dysfunction.
authors.affiliation: Dipartimento di Medicina Interna e Specialità Mediche, La Sapienza Università di Roma, Rome, Italy. francesco.angelico@uniroma1.it
authors.forename: Francesco
authors.initials: F
authors.lastname: Angelico
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Loffredo
authors.forename: Pasquale
authors.initials: P
authors.lastname: Pignatelli
authors.forename: Teresa
authors.initials: T
authors.lastname: Augelletti
authors.forename: Roberto
authors.initials: R
authors.lastname: Carnevale
authors.forename: Antonio
authors.initials: A
authors.lastname: Pacella
authors.forename: Fabiana
authors.initials: F
authors.lastname: Albanese
authors.forename: Ilaria
authors.initials: I
authors.lastname: Mancini
authors.forename: Serena
authors.initials: S
authors.lastname: Di Santo
authors.forename: Maria
authors.initials: M
authors.lastname: Del Ben
authors.forename: Francesco
authors.initials: F
authors.lastname: Violi
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000975:Antioxidants / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000473:pathology; D015992:Body Mass Index; D016001:Confidence Intervals; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000178:diet therapy* / Q000473:pathology; D019255:NADPH Oxidases / Q000096:biosynthesis*; D009752:Nutritional Status; D010045:Outpatients; D018384:Oxidative Stress; D013223:Statistics as Topic; D015431:Weight Loss
chemical_list: D000975:Antioxidants; D019255:NADPH Oxidases