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Dietary Modification - Mediterranean Diet

Mediterranean diet reduces endothelial damage and improves the regenerative capacity of endothelium📎

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Abstract Title:

Mediterranean diet reduces endothelial damage and improves the regenerative capacity of endothelium.

Abstract Source:

Am J Clin Nutr. 2011 Feb;93(2):267-74. Epub 2010 Dec 1. PMID: 21123460

Abstract Author(s):

Carmen Marin, Rafael Ramirez, Javier Delgado-Lista, Elena Maria Yubero-Serrano, Pablo Perez-Martinez, Julia Carracedo, Antonio Garcia-Rios, Fernando Rodriguez, Francisco Miguel Gutierrez-Mariscal, Purificación Gomez, Francisco Perez-Jimenez, Jose Lopez-Miranda

Article Affiliation:

Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofía University Hospital, University of Cordoba, Córdoba, Spain.

Abstract:

BACKGROUND: Endothelial dysfunction is a fundamental step in the atherosclerotic disease process. Activation or injury of the endothelium leads to a variety of inflammatory disorders, including the release of microparticles. Endothelial progenitor cells may contribute to the maintenance of the endothelium by replacing injured mature endothelial cells.

OBJECTIVE: We studied the influence of dietary fat on the release of endothelial microparticles (EMPs) and endothelial progenitor cells (EPCs) in elderly subjects.

DESIGN: Twenty healthy, elderly subjects (10 men and 10 women) consumed 3 diets following a randomized crossover design, each for 4 wk: a saturated fatty acid diet; a low-fat, high-carbohydrate diet; and a Mediterranean diet (MedDiet) enriched in monounsaturated fatty acids. We investigated total microparticles, EMPs from activated endothelial cells (activated EMPs), EMPs from apoptotic endothelial cells (apoptotic EMPs), EPCs, oxidative stress variables, and ischemic reactive hyperemia (IRH).

RESULTS: The MedDiet led to lower total microparticle, activated EMP, and apoptotic EMP concentrations and higher EPC numbers than did the other diets (P<0.001). We detected lower superoxide dismutase activity (P<0.001), a higher plasmaβ-carotene concentration (P<0.001), and lower urinary isoprostane and plasma nitrotyrosine concentrations after consumption of the MedDiet than after consumption of the other 2 diets (P<0.05). Furthermore, the occurrence of IRH was higher after consumption of the MedDiet than after consumption of the other 2 diets (P<0.05).

CONCLUSION: Consumption of the MedDiet induces a reduction in endothelial damage and dysfunction, which is associated with an improvement in the regenerative capacity of the endothelium, in comparison with 2 other diets.


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