IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
High-fructose intake induce vascular remodeling in apolipoprotein e deficient mice.
Autor/es:
CANNIZZO, BEATRIZ; LEMBO, CARINA; CRUZADO, MONTSERRAT; CASTRO, CLAUDIA
Lugar:
Córdoba
Reunión:
Congreso; XLIV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB); 2008
Institución organizadora:
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB)
Resumen:
HIGH-FRUCTOSE INTAKE INDUCE VASCULAR REMODELING IN APOLIPOPROTEIN E DEFICIENT MICE Cannizzo Beatriz, Lembo Carina, Cruzado, Montserrat y Castro, Claudia. Laboratorio de Biología Vascular IMBECU-CONICET y Facultad de Ciencias Médicas, UNCuyo, Mendoza Fructose fed (FF) mice provides a model of dietary-induced insulin resistance, which has been used to assess the pathophysiological mechanisms of the cardiovascular changes associated to the metabolic syndrome. We hypothesized that chronic administration of fructose (10% in drinking water) to a murine model of atherosclerosis, apolipoproteína E deficient mice (apoE-/-), which develops hypercholesterolemia, would alter their metabolic profiles and result in arterial wall remodeling. Male ApoE-/- mice and their control C57BL/6 wild type were used (6-8 in each group). After 6 weeks fructose administration metabolic and morphometric variables were measured. Similar high cholesterol level was measured on both FF ApoE-/- and ApoE-/- group, instead, fasting glucose was significantly elevated only in FFApoE-/- group. The media cross-sectional area of vascular wall in the FF ApoE-/- group compared with ApoE-/- was significantly increased (67606,6 μm2 ± 8908,3 vs 40317,0 μm2 ± 7126,2 p=0,016) with a trend toward higher media/lumen ratio (1,3 ±0,61 vs. 0,40 ± 0,04). Tissue remodeling by matrix metalloproteinases (MMPs) is postulated to be involved in the pathogenesis of atherosclerosis. We found an increase of MMP-9 expression in FFApoE-/- arterial wall. These data support the hypothesis that hyperglycemia