Dietary Fats, Prostanoids and Arterial Thrombosis by Gerard Hornstra M.D. (auth.)

By Gerard Hornstra M.D. (auth.)

Knowledge of mechanisms interested by the pathogenesis of occlusive arterial dis­ eases is prime for the layout of prevention and therapy. a chain of experiences in keeping with in vitro investigations, the experimental animal and the man or woman have slowly elevated our figuring out of cardiovascular ailments and unveiled their secrets and techniques to us. over the past 60 years it's been regularly assumed that nutritional fat and lipids and the prevalence of atherosclerosis are heavily similar. but, whether epidemiological reports essentially point out the life of an organization among the quantity of composition of nutritional lipids and morbidity and mortality of aerobic­ vascular affliction, our easy wisdom on reason and impression continues to be hidden in a cloud of uncertainty. the current ebook discusses the relation among nutritional lipids and arterial throm­ bosis, which latter strategy has been saw within the coronary arteries in as much as ninety% of topics with acute myocardial infaction. during this quantity Dr. Hornstra, who has occupied himself with thrombosis examine with never-failing enthusiasm, nice ability and demanding procedure for the final fifteen years, attempts to set up attainable hyperlinks among lipid metabolism and thrombosis. His literature reviews are finished and his investigations are amazing in that they offer a brand new size and a brand new technique to analyze of lipids and thrombosis.

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Extra info for Dietary Fats, Prostanoids and Arterial Thrombosis

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The released AA is peroxidized to form PGG 2, a cyclic hydroperoxide [330,626]. The enzyme involved (prostaglandin endoperoxide synthase, or cyclo-oxygenase, CO) is located at the cytoplasmatic side of the endoplasmatic reticulum [773]. Since CO has also a peroxidase activity [562,640], PGG 2 is immediately converted into PGH 2. The CO-enzyme system is present in virtually all tissues and is a so-called selfdestructive enzyme [477] because it is inactivated by the compound it produces [223]. It is inhibited by non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and indomethacin [244, 703, 764, 857].

Therefore, membrane fluidity may determine, at least in part, receptor availability and efficiency and, as a result, modulate a great number of membrane-located processes. Membrane fluidity is affected by the relative proportion of the different phospholipid classes, the chain length and degree of un saturation of their fatty acid residues and the membrane cholesterol content [182,424,471]. Since these latter two factors can be influenced by diet, one may expect a dietary effect on membrane fluidity and on the processes depending on it.

Therefore, endogenously formed polyunsaturated fatty acids can be classified as members of the (n-9)- or the (n-7)-family. 5 shows the major steps of the biosynthesis of these families. The desaturase enzyme system is stimulated by dietary carbohydrates and SAFA's. Insulin has also been reported to have a stimulating effect, which is most probably indirect. To attain an optimum activity, the desaturase enzyme complex requires the presence of certain cytoplasmic proteins. These proteins most probably act as fatty-acid binding proteins and may regulate the supply of fatty acids (or its CoA-esters) to the enzyme.

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