scholarly journals The effect of oil phytopreparations on the lipid status in an experiment

2012 ◽  
Vol 93 (4) ◽  
pp. 561-563
Author(s):  
A K Berdgaleeva ◽  
N T Aldiyarova ◽  
S K Sakhanova

Aim. To study the effect of oil extracts of the burdock root and elecampane on the lipid profile in an experimental model of cholesterolosis. Methods. Experiments were performed on 60 white nonlinear rats, weighing 180-300 g. The oil extract from the burdock root was administered intragastrically at a dose of 2.5 ml/kg, and an extract from the root of elecampane - at a dose of 1.0 ml/kg during the last 30 days on the background of a cholesterol diet. After removal of the animals from the experiment the levels of cholesterol, triglycerides, high and low density lipoproteins, phospholipids, free fatty acids were determined in the blood serum and in liver homogenates with the use of standardized sets. Results. Administration of oil extracts of the burdock root and elecampane on the background of a cholesterol diet resulted in a significant reduction in serum cholesterol level by average of 1.48 times, triglycerides level - by 1.9 times, low-density lipoproteins level - by 1.8 times, as well as in a significant increase in the level of high-density lipoproteins on average by 1.5 times compared with the pathology model. In the same conditions the oil extracts of the burdock root and elecampane significantly increased the phospholipid content in the liver tissue by 1.4 and 1.7 times, respectively, the content of free fatty acids - by 2 times in average, the content of esterified cholesterol - by about 1.5 times as compared with the pathology model. Conclusion. The studied oils have a unidirectional positive effect on the lipid content in blood serum and liver in an experimental cholesterolosis; the oil extract from the root of elecampane has a more pronounced effect.

2014 ◽  
Vol 13 (1) ◽  
pp. 67-72 ◽  
Author(s):  
A. V. Ratkin ◽  
O. A. Kaidash ◽  
V. V. Ivanov ◽  
A. I. Vengerovsky ◽  
S. M. Adekenov ◽  
...  

Objective: study sesquiterpene lactones grosshemin and grossmisin lipid-lowering properties on the model of acute hyperlipidemia induced by ethanol in rats.Materials and methods. Rats during 7 days injected into the stomach grosshemin and grossmisin in a dose 10 mg/kg or reference drug nicotinic acid in a dose 25 mg/kg. Hyperlipidemia caused by single introduction of ethanol into the stomach in a dose 5 g/kg. In blood serum of tail vein measured the triacylglycerols, total cholesterol, high density and low density lipoproteins cholesterol, also the level of free fatty acids. Calculated the ratio of high density lipoproteins cholesterol to the amount of low density lipoproteins cholesterol and the index of atherogenicity.Results. A single dose of ethanol increased serum level of triacylglycerols in 1.9 times, free fatty acids – in 3.2 times, low density lipoproteins – on 44% in comparison with the intact animals indices. It shows the development of acute hyperlipidemia. Serum total cholesterol, high density lipoproteins cholesterol and the index of atherogenicity were not changed. Course sesquiterpene lactones grosshemin and grossmisin introduction against the background of acute hyperlipidemia was accompanied by a decrease in the serum of triacylglycerols levels respectively by 19.8% and 34.1%. Nicotinic acid lowered the content of triacylglycerols by 42.4%. Grosshemin and nicotinic acid reduced the increased level of free fatty acids in the blood serum by 60.7–67.9%. Grossmisin and nicotinic acid decreased by 14.6–17.2% of total cholesterol in the blood serum. In acute hyperlipidemia grosshemin and grossmisin reduced low density lipoproteins cholesterol by 17.6% and 20%, respectively, nicotinic acid – by 15.7%. Both of sesquiterpene lactone and nicotinic acid did not modify the content of high density lipoproteins cholesterol. When introduction grosshemin, grossmisin and nicotinic acid ratio of high density lipoproteins cholesterol to the amount of low density lipoproteins cholesterol significantly increased by 42.8%, 38,6% and 22.1% respectively.Conclusion. Sesquiterpene lactones grosshemin and grossmisin posses hypolipidemic effect in acute experimental hyperlipidemia caused by the ethanol introduction. Lactones normalize many indices of lipid metabolism, which can be caused by different biochemical targets of these molecules. Lactones, as nicotinic acid, in the model of acute hyperlipidemia decrease in blood serum triacylglycerols, total cholesterol, and low density lipoproteins cholesterol content. Grosshemin and nicotinic acid also reduce the free fatty acids level.


1962 ◽  
Vol 203 (5) ◽  
pp. 914-918 ◽  
Author(s):  
P. J. Nestel ◽  
A. Bezman ◽  
R. J. Havel

Palmitate-9, 10-H3 and linoleate-1-C14 were infused simultaneously into intact dogs as albumin-bound free fatty acids or as esterified fatty acids in chylomicrons. Linoleate bound to albumin was removed more rapidly from the plasma and was incorporated more extensively into triglycerides of very low density lipoproteins of plasma than palmitate. Both linoleate and palmitate were incorporated more slowly into triglyceride fatty acids of low density and high density lipoproteins than into those of very low density lipoproteins. When chylomicrons obtained separately from dogs fed palmitate-9, 10-H3 with milk fat and linoleate-1-C14 with corn oil were mixed and infused into recipients, the rates of removal from the blood of both triglycerides and phospholipids of the two populations of chylomicrons differed, but this did not seem to depend on their chemical composition. Linoleate derived from chylomicron triglycerides disappeared from hepatic triglycerides and phospholipids more rapidly than palmitate and was incorporated more extensively into plasma lipids. Palmitate and linoleate were incorporated in equivalent amounts into circulating free fatty acids, but more linoleate was found in lipids of adipose tissue.


1980 ◽  
Vol 94 (3) ◽  
pp. 503-516 ◽  
Author(s):  
J. E. Storry ◽  
P. E. Brumby ◽  
B. Tuckley ◽  
V. A. Welch ◽  
D. Stead ◽  
...  

SummaryEffects of 0, 1·7, 3·3 or 5·0 kg/day of a protected soya bean – tallow supplement, incorporated into a hay:concentrate diet (25:75) and fed ad libitumto Friesian cows, on intake and digestion of fatty acids, on output of milk fatty acids and on blood lipoprotein composition were measured.Most of the increased intake of fatty acids, approximately 1 kg/day, was accounted for by increased intakes of C16:0, C18:0 and C18:1. At low intakes, amounts of all fatty acids apparently digested were linearly related to their respective intakes. At high intakes of C16 and C18 acids, curvilinear relationships were established.Yield of total milk fat was related positively to dietary intakes of total fatty acid and carbohydrate and negatively to live-weight change. Yields of short and intermediate chain acids in milk, synthesized within the mammary gland, were negatively correlated and yields of C18 fatty acids positively correlated with respective dietary intakes of these acids. Decreased proportions of C4–16 and increased proportions of C18:0 and C18:1 fatty acids in milk were associated with increased protected tallow in the diet. Yields of C16:1 and C18:1 were positively related to corresponding outputs of saturated acids and negatively to weeks of lactation. The proportion of C18:1 in milk was positively related to the corresponding proportion of C18:0.The increased intake of fatty acids resulted in increased concentrations of very low density lipoproteins (VLDL, d < 1·019 g/ml), low density lipoproteins (LDL1 + LDL2, 1·019 < d < 1·06 g/ml), high density lipoproteins (d > 1·060 g/ml) and serum free fatty acids. Most of the increase in low density lipoproteins was accounted for by a very large increase in LDL1, whose proportion increased from 17 to 75% (2 to 22% of total serum lipid). The proportion of triglyceride in the combined low density lipoprotein fraction decreased from 11 to 2% whilst phospholipids increased from 29 to 36%. These changes were attributed to the increased proportion of LDL1 present.The proportions of VLDL and LDL triglyceride taken up by the mammary gland averaged 0·79 and 0·34 respectively. The proportion of VLDL+LDL triglyceride taken up by the gland decreased with increased amounts of fatty acid digested. Yields of C18 fatty acids in milk tended to be positively related to apparent uptakes of VLDL triglyceride and to VLDL C18 fatty acids, but negatively related to apparent uptakes of LDL triglycerides and LDL C18 fatty acids. It is suggested that the increased LDL1 resulted from the utilization of VLDL triglyceride for milk fat formation.Protected lipid feeding increased the proportion of C14:0, C16:0 C16:1 and C18:1 and decreased the proportions of C14:1 and C18:0 fatty acids in jugular serum triglycerides. Similar changes were observed in jugular VLDL triglycerides. Differences in the compositions of VLDL and LDL triglycerides across the mammary gland were observed and attributed either to selective uptake or to interchange of fatty acids between triglycerides and free fatty acids.


1978 ◽  
Vol 176 (1) ◽  
pp. 169-174 ◽  
Author(s):  
P Thomopoulos ◽  
M Berthelier ◽  
D Lagrange ◽  
M J Chapman ◽  
M H Laudat

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.


1990 ◽  
Vol 36 (12) ◽  
pp. 2109-2113 ◽  
Author(s):  
R Siekmeier ◽  
W März ◽  
W Gross

Abstract Recently, polyanion precipitation assays for low-density lipoprotein (LDL)-cholesterol have been found to underestimate their analyte in normolipidemic samples (Siekmeier et al., Clin Chim Acta 1988;177:221-30). Therefore, accuracy, specificity, and interference by nonesterified fatty acids have been studied for three precipitants (obtained by heparin, dextran sulfate, or polyvinyl sulfate precipitation). At normal concentrations of LDL, precipitation is incomplete, whereas it is nearly quantitative at high concentrations of LDL. The polyvinyl sulfate reagent markedly responds to variations in the amount of non-LDL protein present in the precipitation mixture. In the dextran sulfate and the polyvinyl sulfate method, but not in the heparin method, the percentages of LDL precipitated notably increase as the concentration of the polyanion compound is decreased. In either assay, very-low-density lipoproteins, but not high-density lipoproteins, are significantly coprecipitated (dextran sulfate 28%, polyvinyl sulfate and heparin 66%) in a concentration-independent fashion. Increased concentrations of nonesterified fatty acids markedly interfere with the dextran sulfate and polyvinyl sulfate assay, but do not much affect results with the heparin reagent.


2019 ◽  
Vol 20 (10) ◽  
pp. 2521 ◽  
Author(s):  
Cristóbal Flores-Castillo ◽  
María Luna-Luna ◽  
Elizabeth Carreón-Torres ◽  
Victoria López-Olmos ◽  
Sara Frías ◽  
...  

Previous studies demonstrated modifications of high-density lipoproteins (HDL) structure and apolipoprotein (apo) A-I catabolism induced by the atorvastatin and fenofibrate combination. However, it remains unknown whether such structural and metabolic changes of HDL were related to an improvement of the HDL-cholesteryl esters (HDL-CE) metabolism. Therefore, we determined the structure of HDL and performed kinetic studies of HDL-CE radiolabeled with tritium in rabbits treated with atorvastatin, fenofibrate, and a combination of both drugs. The atorvastatin and fenofibrate combination increased the HDL size and the cholesterol and phospholipid plasma concentrations of the largest HDL subclasses. Moreover, the relative amount of unsaturated fatty acids contained in HDL increased, in detriment of saturated fatty acids as determined by gas chromatography–mass spectrometry. The transfers of cholesteryl esters (CE) from HDL to very low-density lipoproteins/low-density lipoproteins (VLDL/LDL) and vice versa were enhanced with atorvastatin, alone or in combination. Moreover, the direct elimination of CE from plasma via VLDL/LDL decreased with fenofibrate, whereas the direct elimination of CE via HDL augmented with the combination treatment. Taken together, the rise of unsaturated fatty acid content and the size increase of HDL, suggest that atorvastatin and fenofibrate induce more fluid HDL particles, which in turn favor an enhanced CE exchange between HDL and VLDL/LDL. Our results contribute to a better understanding of the relationship between the structure and function of HDL during the use of anti-dyslipidemic drugs.


Sign in / Sign up

Export Citation Format

Share Document