INVESTIGADORES
JEREZ Susana Josefina
congresos y reuniones científicas
Título:
High fat diet-induced metabolically obese and normal weight rabbit model shows early vascular dysfunction. Role of cyclooxygenase-2 in normal oxidative status
Autor/es:
ALARCÓN, GABRIELA; ROCO, JULIETA; MEDINA, ANALIA; MEDINA, MIRTA; PERAL, MARIA; JEREZ, SUSANA
Lugar:
Buenos Aires
Reunión:
Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017
Resumen:
Association between obesity and vascular dysfunction has been widely probed. However, mechanisms of vascular changes in individuals with normal weight and clinical characteristics of metabolic syndrome (MS) have not been described so far. The aim of the present work was to evaluate endothelial function and vascular reactivity in a metabolically obese and normal weight (MONW) rabbit model developed by feeding animals on a high fat diet (HFD). Methods: male rabbits were fed either regular diet (CD) or 18% fat in regular diet (HFD) by 6 weeks. Results: HFD induced glucose intolerance (CD:140±5 mg/dl vs HFD:163±4 mg/dl), increased fasting glucose (CD: 102±6 mg/dl v HFD: 126±5 mg/dl), triglycerides(CD: 112±6 mg/dl v HFD: 193±5 mg/dl), C reactive protein (CD: 5.1±0.9 mg/dl v HFD: 22±3 mg/dl), visceral abdominal fat (CD: 0.29±0.05 % vs HFD: 2.3±0.1 %) , TyG index (product of the fasting blood glucose and TG levels, CD: 8.27±0.22 vs HFD: 9.28±0.11) and decreased HDL-cholesterol (CD: 54±4 mg/dl vs HFD: 23±3 mg/dl) and plasma nitrites (CD: 1752±784 nmoles/l vs HFD: 324±109 nmoles/l). No differences were found in body weight, TBARS and Glutathione serum levels between the two diet groups. In aortic rings, isometric contractions measurement showed that HFD: a) reduced the acetylcholine relaxation, effect reversed by NS398 (cyclooygenase-2 inhibitor) and SC560, (cyclooxygenase-1 inhibitor); b) increased the contractile response to norepinephrine and KCl; c) improved the angiotensin II-potency, effect reversed by NS398 and SQ 29538 (TP receptor blocker). Immunohistochemistry and western blot showed cyclooxygenase-2 expression only in arteries from HFD rabbits. Conclusions: HFD induced vascular dysfunction in a model of MONW. Cyclooxygenase-2 up regulation may account for these functional alterations. Considering that normal oxidative status was found in our MONW model inflammatory process may account for the metabolic alterations in early stages of the MS.