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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Ciencias Cardiovasculares > Enfermedad vascular hipertensiva > DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista >

Is leptin involved in phagocytic NADPH oxidase overactivity in obesity? Potential clinical implications
Autor(es) : Fortuño, A. (Ana)
Bidegain, J. (J.)
Baltanas, A. (Ana)
Moreno, M.U. (María Ujué)
Montero, L. (Laura)
Landecho, M.F. (Manuel F.)
Beloqui, O. (Óscar)
Diez, J. (Javier)
Zalba, G. (Guillermo)
Palabras clave : Leptin
NADPH oxidase
Obesity
vascular remodeling
Fecha incorporación: 2010
Editorial : Lippincott Williams & Wilkins
Versión del editor: http://journals.lww.com/jhypertension/pages/articleviewer.aspx?year=2010&issue=09000&article=00023&type=abstract
ISSN: 1473-5598
Cita: Fortuño A, Bidegain J, Baltanas A, Moreno MU, Montero L, Landecho MF, et al. Is leptin involved in phagocytic NADPH oxidase overactivity in obesity? Potential clinical implications. J Hypertens 2010 Sep;28(9):1944-1950.
Resumen
OBJECTIVES: Hyperleptinemia and oxidative stress play a major role in the development of cardiovascular diseases in obesity. This study aimed to investigate whether there is a relationship between plasma levels of leptin and phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and its potential relevance in the vascular remodeling in obese patients. METHODS: The study was performed in 164 obese and 94 normal-weight individuals (controls). NADPH oxidase activity was evaluated by luminescence in phagocytic cells. Levels of leptin were quantified by ELISA in plasma samples. Carotid intima-media thickness (cIMT) was measured by ultrasonography. In addition, we performed in-vitro experiments in human peripheral blood mononuclear cells and murine macrophages. RESULTS: Phagocytic NADPH oxidase activity and leptin levels were enhanced (P < 0.05) in obese patients compared with controls. NADPH oxidase activity positively correlated with leptin in obese patients. This association remained significant in a multivariate analysis. cIMT was higher (P < 0.05) in obese patients compared with controls. In addition, cIMT also correlated positively with leptin and NADPH oxidase activity in obese patients. In-vitro studies showed that leptin induced NADPH oxidase activation. Inhibition of the leptin-induced NADPH oxidase activity by wortmannin and bisindolyl maleimide suggested a direct involvement of the phosphatidylinositol 3-kinase and protein kinase C pathways, respectively. Finally, leptin-induced NADPH oxidase activation promoted macrophage proliferation. CONCLUSIONS: These findings show that phagocytic NADPH oxidase activity is increased in obesity and is related to preclinical atherosclerosis in this condition. We also suggest that hyperleptinemia may contribute to phagocytic NADPH oxidase overactivity in obesity.
Enlace permanente: http://hdl.handle.net/10171/17925
Aparece en las colecciones: DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista
DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista

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