Effect of the prolonged high-fat diet on the fatty acid metabolism in rat blood and liver
1 A.V. Zhirmunsky Institute of Marine Biology of the Far East Branch of the Russian Academy of Sciences, Palchevskogo str., 17, 690041 Vladivostok, Russia
2 School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia
3 Vladivostok Branch of the Far Eastern Center of Physiology and Pathology of Respiration of SB RAMN - Institute of Medical Climatology and Rehabilitative Treatment, Vladivostok, Russia
Lipids in Health and Disease 2014, 13:49 doi:10.1186/1476-511X-13-49Published: 16 March 2014
Contradictory data on consequences of prolonged high-fat diet requires a detailed study of the influence of nutritional high-fat load mechanisms on the peculiarity of lipid metabolism in blood and liver. The present study was undertaken to investigate the fatty acid composition of polar and neutral lipids of the blood plasma, erythrocytes and liver in Wistar rats under the conditions of a prolonged high-fat diet.
The study was conducted on 60 adult white male Wistar rats. The animals were fed on a high-fat diet consisted of the beef fat and cholesterol (19% and 2% of the total diet, respectively) up to 180 days. The fatty acid composition of the polar and neutral lipids of plasma, erythrocytes and liver were analyzed by the gas chromatography. Statistical data processing was performed by the methods of descriptive statistics with Statistica 6.0.
The prolonged unbalanced diet rich in cholesterol and saturated fatty acids resulted in compensatory biosynthesis of the fatty acids in the rat’s liver, the inhibition of synthesis of apoproteins and lipoproteins, disruption of the active transport of fatty acids to tissue cells. This launched the accumulation of 20:4n-6, 20:5n-3, 22:5n-3, and 22:6n-3 in the liver and blood plasma and deficiency of 18:2n-6, 20:5n-3 and 22:6n-3 in the erythrocytes.
Adaptive adjustment of lipid metabolism un0064er conditions of the high-fat diet induced inhibition of the formation of lipoproteins (VLDL cholesterol) in the liver, compensatory synthesis of 18:1n-9, 20:5n-3, and 20:3n-6 with primary esterification of PUFA n-3 series to neutral lipids.