Relative abundance of animal protein in diet: the initiator of the atherosclerotic process

Abstract

In the presented atherosclerosis genesis and development hypothesis relative abundance of animal protein in diet is assumed as the initiator of the process. Relative abundance of dietary protein causes exhaustion of ornithine cycle resources in hepatocytes. Unreacted ammonia (NH3) inhibits ferments of the respiratory chain; electrons transmit directly to oxygen, and reactive oxygen species (ROS) develop in hepatocytes. It results in lipid peroxygenation in cells of endothelial reticulum and in apolipoproteins conformational changes. From hepatocytes oxidized VLDL and oxidized HDL containing active malondialdehyde (MDA) release into blood. Apo-B100, apo-C-II, and apo-A-I conformational changes cause development of dyslipidemias. MDA of oxidized lipoproteins damages membranes of endotheliocytes with endothelial dysfunction genesis. Oxidized apolipoprotein apo-B100 provokes the immune-inflammatory response in the vessel wall. During a longtime receiving of oxidized lipoprotein apo-B100, foam cells develop as well as atherosclerotic changes with their progression leading to angina pectoris and myocardial infarction. MDA of oxidized lipoproteins also damages membranes of erythrocytes and those of thrombocytes causing microcirculation disorder in tissues and enhanced adhesion respectively. The presented hypothesis covers all the main stages of atherogenesis.