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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postprandial response to three test meals provided during a single day was investigated in subjects with either the apo E3/3 phenotype (n = 8), or the apo E4/3 phenotype (n = 4), who had LDL-C greater than 160 mg/dl. Vitamin A (60,000 U/m2) was ingested with the first meal and retinyl palmitate determined four hours later. Triglyceride and total cholesterol concentration were determined on whole plasma and total cholesterol and free cholesterol determined following single spin ultracentrifugation (d less than 1.006 g/ml) and dextran precipitation of the d greater than 1.006 fraction to separate apoprotein-B containing lipoproteins. Fasting values revealed significantly lower HDL-cholesterol ester (p less than 0.03) and HDL3-cholesterol ester (p less than 0.03) and significantly greater HDL-free cholesterol (p less than 0.03) and HDL3-free cholesterol (p less than 0.02) in subjects with the E4/3 phenotype. Four hour postprandial HDL and HDL3 cholesterol ester increased significantly more (p less than 0.05) in E4/3 patients and HDL and HDL3 free cholesterol decreased significantly more (p less than 0.05) in E4/3 subjects. Eight-hour postprandial change values maintained the significant HDL3-cholesterol ester and free cholesterol difference, and, revealed a significantly greater triglyceride rich lipoprotein cholesterol ester reduction (p less than 0.01) in the E4/3 group. Individuals with the apolipoprotein E4/3 phenotype reveal significant differences in postprandial lipemia compared to individuals with the E3/3 phenotype, and, postprandial lipemia following multiple meals reveals differences not apparent from responses to a single meal.
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PMID:The effect of apolipoprotein E isoform difference on postprandial lipoprotein in patients matched for triglycerides, LDL-cholesterol, and HDL-cholesterol. 175 Aug 4

To test the hypothesis that conditioning with a practical dose of fish oil will reduce postprandial lipemia, 25 healthy men were matched according to levels of fasting plasma triacylglyceride and allocated to 6 weeks of either fish oil or olive oil supplements (5 g/day). After a 12-hour overnight fast at the termination of the study period, the subjects were given a standard test meal containing 89% of energy as fat (0.73 g fat/kg body wt, polyunsaturated to saturated fat ratio = 0.4). Vitamin A (429 retinol equivalents/kg body wt) was included to endogenously label the chylomicrons. Venous blood samples were obtained before the test meal and hourly thereafter for 8 hours. Chylomicrons were separated by ultracentrifugation, plasma triacylglyceride concentration was determined enzymatically, and retinyl ester levels were measured by liquid chromatography. Postprandially, the fish oil-fed group exhibited mean total and chylomicron triacylglyceride concentrations that were significantly (p less than 0.05) less than those of the olive oil-fed group. Both the fish oil- and olive oil-fed groups had similar rises in chylomicron retinyl esters during the first 2 hours, but after this time the postprandial response of the fish oil-fed group was consistently and significantly (p less than 0.05) less than the response of the olive oil-fed group. Our results suggest that improvement in lipemic response, whether due to enhanced chylomicron clearance or decreased chylomicron entry into the plasma pool, can be achieved at a much lower intake of fish oil than previously reported.
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PMID:Moderate fish oil intake improves lipemic response to a standard fat meal. A study in 25 healthy men. 202 89

Advances in our knowledge of the microsomal metabolism of ethanol enable us to understand a number of complications that develop in the alcoholic. After chronic ethanol consumption, microsomal ethanol-oxidizing system (MEOS) activity increases with an associated rise in microsomal cytochrome P-450, including a form different from that induced by phenobarbital and methylcholanthrene and which has a high affinity for ethanol, as shown in reconstituted systems. The role of this MEOS in vivo and its increase after chronic ethanol consumption was most conclusively shown in alcohol dehydrogenase-negative deer mice. Microsomal induction is also associated with enhanced metabolism of other drugs, resulting in metabolic drug tolerance. Furthermore, there is increased conversion to toxic metabolites of known hepatotoxic agents (such as CCl4), which may explain the enhanced susceptibility of alcoholics to the toxicity of industrial solvents. Furthermore, the ethanol-induced form of cytochrome P-450 has a high capacity for the conversion to toxic metabolites of some commonly used drugs, such as acetaminophen, and also carcinogens, such as dimethylnitrosamine which is activated at concentrations much lower than those required for other microsomal inducers. Moreover, catabolism of retinol is accelerated through a newly discovered microsomal pathway, thereby contributing to hepatic vitamin A depletion and possibly vitamin A toxicity. There is also induction of microsomal enzymes involved in lipoprotein production, resulting in hyperlipemia. Contrasting with the chronic effects of ethanol consumption, acutely, ethanol inhibits the metabolism of other drugs through competition for an at least partially shared microsomal detoxification pathway.
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PMID:Microsomal ethanol-oxidizing system. 310 31

In 20 adult patients suffering from hyperlipidaemia we measured the lipid composition of erythrocyte membrane, the glutathione peroxidase activity in both erythrocytes and platelets, the production of malondialdehyde by platelets stimulated with thrombin, as well as the level of plasma selenium, retinol and alpha-tocopherol, before and after 8 weeks of fish oil supplementation (20 ml daily). We noted a remarkable reduction in plasma triglycerides which was associated with a significant decrease in blood pressure; moreover, we noted a reduction in the amount of arachidonic acid compensated by an increment of omega-3-fatty acid (particularly eicosapentaenoic and docosahexaenoic acids). The dietary supplementation with fish oil was associated with a significant increase in glutathione peroxidase activity in both erythrocytes and platelets. On the contrary, the production of malondialdehyde, which was originally higher than normal in hyperlipidaemics, was inhibited significantly after fish oil (p less than 0.001). Whereas no changes were observed in the concentration of plasma selenium and alpha-tocopherol, an increment of plasma retinol occurred. These data indicate that in hyperlipidaemics there is a proaggregant status; this situation may be normalized by using a dietary supplementation of fish oil; the increase of polyunsaturated fatty acids on the cell membrane, with a possible increment of the formation of lipoperoxides, induced by fish oil, is compensated by an increased activity of the scavenger enzyme glutathione peroxidase.
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PMID:Effects of dietary fish oil on malondialdehyde production and glutathione peroxidase activity in hyperlipidaemic patients. 320 Oct 98

Some epidemiological studies have suggested an inverse relation between serum cholesterol concentration and mortality from cancer. Two hypotheses that might explain such a relation were investigated. To assay potentially deleterious effects of hypocholesterolaemia on cell membranes the lipid content and fluidity of blood mononuclear cells were measured in healthy male volunteers with a wide range of serum cholesterol concentration (3.2-10.0 mmol/l (124-387 mg/100 ml)). Fluidity, unesterified cholesterol content, and the ratio of cholesterol to phospholipid were unrelated to serum cholesterol and to low density lipoprotein cholesterol concentrations. Similar measurements were made on fibroblasts and mononuclear cells incubated with a range of concentrations of low density lipoprotein; fluidity was altered only at extremely low concentrations, suggesting that changes in cell membranes are unlikely to occur at serum cholesterol concentrations attainable by dietary or drug treatment of hyperlipidaemia. In the same population direct relations were confirmed between low density lipoprotein concentration and plasma concentrations of retinol and beta carotene. This is compatible with the suggestion that an association between low cholesterol concentration and cancer may be secondary to a relation between low retinoid concentrations and cancer.
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PMID:Hypocholesterolaemia and non-cardiovascular disease: metabolic studies on subjects with low plasma cholesterol concentrations. 640 7

Chronic cholesterol feeding has been shown to produce abnormal plasma lipoproteins in a variety of experimental animals and man. In order to explore the role of the intestine in the production of these abnormal lipoproteins, rats were chronically fed a diet containing 1% cholesterol and 10% olive oil and were compared to control animals, fed either normal chow or normal chow containing 10% olive oil. Mesenteric lymph lipoproteins from fasting lymph and from lymph obtained after acutely infusing cholesterol and olive oil were examined and compared to plasma lipoproteins from these animals. There were no differences in apoA-I output, cholesterol output, or distribution in lymph lipoproteins between the two groups of controls. The cholesterol-olive oil diet produced a mild hyperlipidemia (plasma cholesterol 81 --> 95 mg/dl, plasma triglyceride 95 --> 162 mg/dl). Plasma lipoprotein electrophoresis revealed an abnormal band with broad beta mobility and a reduction in HDL. Lipid analysis of ultracentrifugally separated fractions demonstrated the appearance of an intermediate density (1.006-1.030 g/ml) lipoprotein in plasma markedly enriched in cholesteryl esters. Analysis of fasting mesenteric lymph from chronically cholesterol-fed animals revealed similar apoA-I, cholesterol, and triglyceride outputs when compared to controls. Although in both groups most of the cholesterol was transported in d < 1.006 g/ml lipoproteins, there was a redistribution of cholesterol transport in d > 1.006 g/ml lipoproteins. In the chronically cholesterol-fed animals, 19% of fasting lymph cholesterol was transported in a lipoprotein of density 1.006-1.030 g/ml, compared to 4% in this density in controls. During the acute infusion of cholesterol and olive oil, the output of lymph apoA-I (226 +/- 20 versus 374 +/- 5 micro g/hr, P < 0.025) and lymph cholesterol (970 +/- 82 +/- 1774 micro g/hr, P < 0.01) was significantly lower in the chronically cholesterol-fed group, despite no significant change in triglyceride outputs (49 +/- 2 versus 58 +/- 7 mg/hr). Analysis of individual lymph lipoproteins from chronically cholesterol-fed animals revealed that significantly less apoA-I and cholesterol was carried in d < 1.006 g/ml lipoproteins than in controls. There was however, both a relative and absolute increase in the cholesterol and apoA-I content of intermediate and low density lymph subfractions. Particularly prominent in lymph from chronically cholesterol-fed animals was a lipoprotein (d 1.006-1.030 g/ml) which was inconsistently found in controls. This particle was rich in cholesterol and contained apoA-I. [(3)H]Retinol infusion studies revealed that this particle contained increased retinyl ester when compared to plasma, suggesting an intestinal origin. These results demonstrate that chronic cholesterol feeding in the rat results in altered mesenteric lymph lipoproteins which may contribute to the abnormalities found in plasma.-Riley, J. W., R. M. Glickman, P. H. R. Green, and A. R. Tall. The effect of chronic cholesterol feeding on intestinal lipoproteins in the rat.
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PMID:The effect of chronic cholesterol feeding on intestinal lipoproteins in the rat. 744 Oct 62

In this study we assessed the acute effects of the consumption of varying amounts of fat and fructose on the magnitude of postprandial lipemia. Subjects were studied after an overnight fast on four separate mornings, ingesting in random order 5, 40, or 80 g fat, or 5 g fat plus 50 g fructose. Vitamin A (36 mg, or 120,000 U retinol) was also given and blood was drawn at frequent intervals over the next 10 h for measurement of triacylglycerol and retinyl palmitate (RP) concentrations in plasma and the Sf > 400 and Sf 20-400 lipoprotein fractions. (Sf denotes flotation units.) In general, the postprandial triacylglycerol response increased in plasma and in both lipoprotein fractions as a function of both the baseline fasting triacylglycerol concentration and the amount of fat ingested. However, no matter how high the fasting plasma triacylglycerol concentration, there was no increase in the postprandial triacylglycerol concentration in plasma or either lipoprotein fraction after the 5-g oral fat load. The results of the measurements of RP concentration were somewhat similar in that there was a dose-dependent increase in the plasma and the Sf > 400 lipoprotein fraction in response to the higher fat loads. However, just the opposite was true in the Sf 20-400 lipoprotein fraction, for which the increase in RP concentration was inversely related to the size of the fat load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of variations in oral fat and carbohydrate load on postprandial lipemia. 1112 69

It has been shown that addition of fructose to an oral fat load results in higher postprandial concentrations of triglyceride. The present study, performed in 11 healthy volunteers, was initiated to see whether the effect of fructose on fat-induced lipemia also involved changes in postprandial concentrations of triglyceride-rich lipoproteins of intestinal origin. Vitamin A was used to label intestinal lipoproteins, and the retinyl palmitate concentrations were determined in plasma and in the Sf > 400 and Sf 20-400 lipoprotein fractions (Sf denotes the Svedberg flotation index). Addition of fructose (50 g) to a standard (40-g oral) fat load resulted in higher postprandial concentrations of triglyceride and retinyl palmitate in plasma and the Sf > 400 lipoprotein fraction (P < 0.001, analysis of variance), and the higher the fasting plasma triglyceride concentration, the greater the magnitude of the fructose effect (r = 0.83, P < 0.002). These data show that triglyceride-rich lipoproteins of intestinal origin play a role in the fructose-induced accentuation of postprandial lipemia.
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PMID:Postprandial triglyceride and retinyl ester responses to oral fat: effects of fructose. 770 20

Familial xanthomatous hypercholesterolemia is a metabolic disorder associated with high LDL levels attributed to a familial defect in LDL receptor activity. We have previously shown that hyperlipoproteinemia of WHHL rabbits, considered to be a model for heritable hypercholesterolemia, was at least partly of exogenous origin. We have though studied retinyl palmitate (RP) levels 12 h after a standardized mixed meal as a simple test to detect abnormalities of intestinal-derived lipoprotein clearance in 22 familial hypercholesterolemic patients with xanthomatosis (13 of them treated by simvastatin, an HMGCoA reductase inhibitor, and 9 not treated), as compared to a control group (n = 12). Total and LDL cholesterol, plasma triglyceride and apo B levels were significantly higher in patients when compared to controls. Mean RP levels appeared higher in familial hypercholesterolemic patients, when compared to controls, with 6 among 22 patients showing clearly high vitamin A levels and 4 borderline values, whereas high triglyceride levels (> 2 g/l) were detected in only 1 patient. No patients within the group with high vitamin A levels showed an apo E2/E2 phenotype. Vitamin A levels correlated with plasma triglycerides in the whole group of subjects (r = 0.50, p < 0.05). No difference was observed in vitamin A distribution between treated and untreated hypercholesterolemic patients. Our results indicate that the clearance of RP-labeled intestinal lipoproteins is delayed in some xanthomatous familial hypercholesterolemic patients as compared with that of controls. These findings suggest that familial xanthomatous hypercholesterolemia may be heterogenous concerning physiopathological mechanisms inducing hyperlipidemia.
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PMID:Familial xanthomatous hypercholesterolemia: abnormal exogenous lipid metabolism evidenced by the vitamin A test. 771 Feb 66

An acute oral fat load produces transient lipemia that is enhanced by the simultaneous ingestion of ethanol. This phenomenon has been reinvestigated in six normal subjects who consumed three different fat loads with and without ethanol. The fat loads consisted of saturated fat, polyunsaturated fat, or polyunsaturated fat enriched with omega-3 (n-3) fatty acids. Each fat load contained retinol as a marker for intestinally derived lipoproteins. Plasma levels of triglycerides, retinyl palmitate, and nonesterified fatty acid species were determined at several time points after consumption. Increasing the size of a saturated fat load increased postprandial lipemia and delayed retinyl palmitate clearance. Postprandial lipemia and plasma retinyl palmitate concentrations were lower when omega-3 or omega-6 (n-6) polyunsaturated fat was substituted for saturated fat. Preprandial ethanol increased postprandial lipemia, an effect that was most profound with the saturated fat load. Concurrently, oral ethanol also increased postprandial retinyl palmitate. Addition of ethanol to the fat loads had no effect on the plasma concentrations of fatty acids derived from peripheral tissue but appeared to decrease the plasma concentration of free fatty acids of dietary origin. These data support the hypothesis that preprandial ethanol is associated with impaired chylomicron hydrolysis that may be due to inhibition of plasma lipoprotein lipase. These findings are important to the search for the molecular mechanism of ethanolic hypertriglyceridemia and to the development of dietary guidelines for its control.
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PMID:Dietary ethanol is associated with reduced lipolysis of intestinally derived lipoproteins. 789 9


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