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Characterizing the effects of the Mediterannean diet on endothelial dysfunction

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Another look at the effects of the Mediterranean diet

The development of atherosclerosis is preceded by increased cytokine release which can be induced by dysfunction of the blood vessel linings. European research has investigated the effects of different fats including mono-unsaturated fatty acids (MUFAs) on this phenomenon.

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It seems as if 'we are what we eat' is gathering research backing more and more. The 'Characterizing the effects of the Mediterranean diet on endothelial dysfunction' (Endomed) project looked at just one important factor linked to the diet, the malfunction of the inner lining of blood vessels. When blood vessel endothelium is operating normally, it performs a number of crucial regulatory processes. These include regulation of blood clotting, assisting the immune system, controlling fluid volume and the concentration of electrolytes. Endothelial dysfunction means that one or more of these functions are disrupted or reduced. Endomed looked particularly at the post-prandial metabolism effects of the fatty acids in the typical Mediterranean diet – during the period after a meal – for developing inflammation-related diseases like type II diabetes and heart disease. Project members have shown that types of dietary fat could even influence gene expression in peripheral blood mononuclear cells (PBMCs). Under certain conditions, PBMCs can be responsible for secretion of pro-inflammatory cytokines. The changes in gene expression seemed to be due to the effects of the different fatty acids on the PBMCs and the different tissues and organs that released several hormones as well as cytokines. The Endomed team focused on the pathways involving nuclear factor kappa-light-chain-enhancer of activated B (NF-kappaB), peroxisome proliferator-activated receptor alpha (PPARa) and the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex, all with links in the inflammatory world. IL1B is a potent pro-inflammatory cytokine released in diabetes type II patients and is regulated by NF-kappaB, for example. Preliminary results showed that the pathways involving the pro-inflammatory agents could well be differentially upregulated by the distinct types of fat in the diet. Upregulation of the genes responsible for these molecules suggest that polyunsaturated fats (PUFAs) and MUFAs might be inducing a post-prandial inflammatory response before a rise in reactive oxygen species (ROS) production. Another strand in the Endomed research followed the activity of monocytes, a type of PBMC, in vivo. PBMCs from healthy and obese individuals were subject to gene expression studies. This time, other candidate genes in relation to inflammation, lipid metabolism and oxidative stress pathways were targeted. Data from these studies can be used to provide nutritional guidelines for the public at large to reduce the burden of diabetes type II and heart disease. Patients suffering from these metabolic disorders may also stand to benefit from adjustments to their overall fat intake as well as type of fat consumed.

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