[Hypertrygliceridemia as a factor of atherogenesis: significance and mechanisms of action].
The aim of the study was to investigate the pattern of lipid and lipoprotein metabolism disturbances in patients with manifested clinical signs of coronary atherosclerosis. There was determined the significance of hypertrigliceridemia as the marker of these disturbances and its connection with other most important factors of atherogenesis such as insulin resistance, systemic inflammation, and oxidative stress, blood lipoprotein modification. The role of excessive alimentary lipid consumption as a factor, which initiates the hypertrigliceridemia development and accompanying activation of the other proatherogenic factors was determined with the use of acute lipid loading. It was established that hypertrigliceridemia is one of the most reliable signs ofatherosclerosis existence but it coincides as a rule with other signs of dislipidemia, a decrease in insulin sensitivity, systemic inflammation and lipid free radical oxidation development. The modification of blood lipoprotein and increase of blood atherogenic potentials were the integral effects of these factors. Significance of hypertrigliceridemia as the factor initiating all these disturbances both in normal volunteers and in examined patients was shown in conditions of acute lipid loading which was accompanied by the development of the whole complex of proatherogenic disturbances. It was established that the development of atherosclerosis is connected with the decrease of lipid tolerance and as a result the same lipid loading was accompanied with proportional increase of both hypertrigliceridemia and connected with it proatherogenic disturbances. The obtained data allowed concluding that hypertrigliceridemia is the factor which can initiate the proatherogenic systemic disturbances which include changes in lipid, lipoprotein and glucose metabolism, the development of insulin resistance, systemic inflammation and oxidative stress. These changes are pathogenically interconnected, capable to amplify one another and induce blood lipoprotein modification with appearance of both proatherogenic and autoantigenic propertries, which stipulate the role of hypertrigliceridemia in atherogenesis.
Ambroskina
V V
VV
Kriachok
T A
TA
Larionov
O P
OP
Bratus'
V V
VV
Talaieva
T V
TV
D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000150:complications* / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood*; D017202:Myocardial Ischemia / Q000097:blood / Q000209:etiology / Q000378:metabolism; D018384:Oxidative Stress
D001786:Blood Glucose; D008054:Lipid Peroxides; D008074:Lipoproteins; D002097:C-Reactive Protein