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

In this study, we have investigated the effects of alimentary lipemia in 15 normotriglyceridemic individuals on high density lipoproteins2 (HDL2) with respect to structure, composition, and substrate efficacy for hepatic lipase in vitro. In the study subjects, HDL2 levels ranged widely from 4.7 to 151.7 mg/dl plasma. HDL2 were isolated in the postabsorptive (pa) state and in the postprandial (pp) state, i.e., 7 h after ingestion of a standard fatty meal. In going from the pa state to the pp state, HDL2 exhibited higher flotation rates and lower densities due to a decreased proportion of protein (38.7----36.2%) and a higher abundance in phospholipid (32.5----34.9%). There was a variable increase in triglyceride at the expense of cholesteryl esters; this increase was correlated positively with the magnitude of pp lipemia (r = 0.69, P less than 0.01) and inversely with HDL2 levels (r = -0.72, P less than 0.01). Hdl2 fractions were incubated with human hepatic lipase in vitro. Product lipoproteins formed from lipolysis of pa-HDL2 and triglyceride-poorer pp-HDL2 were reduced in phospholipid content (by 25 and 50%, respectively) but remained in the size and density range of native HDL2. By contrast, a major fraction of triglyceride-richer pp-HDL2 was converted to particles with density, size, and apoprotein composition of native HDL3. Changes consistent with these findings in vitro were observed in vivo also, where 15 h postprandially, individuals with high-level lipemia showed a decrease in HDL2 and rise in HDL3, while those with lower-level lipemia did not. This study indicates that the magnitude of postprandial lipemia determines the proportion of triglyceride in pp-HDL2, which in turn determines whether or not HDL2 are converted to HDL3 by hepatic lipase action.
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PMID:Postprandial lipemia. A key for the conversion of high density lipoprotein2 into high density lipoprotein3 by hepatic lipase. 643 39

Amounts of plasma lipids, apolipoprotein AI (apo AI) and apolipoprotein E (apo E) were measured in streptozotocin-induced diabetic rats. Plasma triglyceride and cholesterol levels of diabetic rats were not significantly different from those of control rats. Plasma apo AI levels of diabetic rats were significantly higher than those of control rats (78.2 +/- 29.3 vs 27.2 +/- 3.4 mg/dl, P less than 0.001), while plasma apo E levels of diabetic rats were significantly lower than those of control rats (4.2 +/- 1.0 vs 13.9 +/- 5.3 mg/dl, P less than 0.001). Insulin treatment (12U/day) of diabetic rats decreased plasma apo AI levels significantly (treated: 32.8 +/- 3.4, untreated: 48.7 +/- 6.2, control: 28.5 +/- 2.4 mg/dl) and normalized plasma apo E levels (treated: 16.1 +/- 1.7, untreated: 5.4 +/- 0.7, control: 15.8 +/- 1.3). Insulin injection (4U/day) to normal rats did not cause any changes in both plasma apo AI and apo E levels. The data indicate that diabetes is not always accompanied by hyperlipidemia, however this inevitably carries apoprotein abnormalities characterized by the high plasma apo AI and low apo E levels, which are reversible with insulin treatment. The changes in the levels of plasma apo AI and apo E could be related to the development of atherosclerosis in diabetes.
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PMID:Reciprocal changes of plasma apo AI and apo E levels in streptozotocin-induced diabetic rats. 644 8

A cyclophosphamide injection to male New Zealand white rabbits induced a pronounced hypertriglyceridemia and a hypercholesterolemia whose concentration was maximal at 16 hr. Different doses were studied. In this hyperlipemia significant changes in plasma lipoprotein fractions appeared: the very low density lipoproteins increased and the high density lipoproteins decreased. Lipid composition showed that HDL cholesterol was very low comparatively to a high VLDL cholesterol. The apoprotein composition of VLDL from treated rabbits was studied and compared to that of normal rabbits. After electrophoresis in urea/polyacrylamide gels, two new apoproteins which resembled those observed in irradiated rabbits appeared. The molecular weight of these proteins was about 10,000, and they focused into three bands with isoelectric points of 6.72, 6.42 and 6.10. Total lipoprotein lipase activity in treated rabbits decreased; it was very low with 32.5 mg/kg. This lipolytic activity remains to be studied after separation of hepatic triacylglycerol lipase and lipoprotein lipase activities by chromatography.
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PMID:Effects of an antimitotic agent (cyclophosphamide) on plasma lipoproteins. 648 48

With the view of examining the serum lipid metabolism-improving action of a new compound, ethyl-2-(4-chlorophenyl)-5-ethoxy-4-oxazole acetate (Y-9738), 900 mg was administered to 47 patients with various diseases associated with hyperlipidemia and/or hypo-HDL (high density lipoprotein)-emia for successive 16 weeks. Serum HDL-cholesterol increased significantly 4 weeks after the administration (mean 11.8%, p less than 0.01). In the patients with hypo-HDL-emia who showed the initial level of 50 mg/dl or less, the degree of increase was more remarkable (mean 16,4%, p less than 0.01), and a significant increase was noted until 12 weeks later. Further, a similar change was noted in respect to serum HDL-phospholipid. The main apoprotein of HDL, apoprotein A (I + II) began to increase significantly 4 weeks after the institution of the administration. At the end of the trial, it increased by mean 31% (p less than 0.01). Y-9738 did not exert any significant effect on serum total cholesterol, triglyceride and phospholipid, but it caused a reduction in so-called atherogenic indexes.
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PMID:Effects of ethyl-2-(4-chlorophenyl)-5-ethoxy-4-oxazole acetate (Y-9738) on the serum lipids of patients with hyperlipidemia and/or hypo-HDL-emia. 654 94

Normal plasma lipid levels do not prevent the infiltration of skin and arterial walls by cholesterol. This does not mean that lipoproteins do not play a role in tissue infiltration which takes place in subjects with normal lipids. Abnormal lipids, an abnormal distribution of atherogenic and non-atherogenic lipids in the blood, a latent hyperlipidemia, the relative proportions of apolipoproteins in circulation or an abnormal composition of the lipoproteins may contribute to this phenomenon. Our studies in subjects with normal lipid levels with xanthelasmata support the hypothesis that the apolipoprotein-B has atherogenic properties. In addition, they suggest that certain isomers of the apolipoprotein-E may also be involved. Preliminary studies in our laboratory using a simple technique of identifying the 6 phenotypes of the apolipoprotein-E suggest that the isomer E2 may favour the appearance of hyperlipidemia when another genetic or environmental factor is present.
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PMID:[Xanthoma and atherosclerosis in the presence of normal plasma lipids]. 665 Oct 70

Autologous 131I-labelled very low density lipoprotein (VLDL) and 125I-labelled low density lipoprotein (LDL) were injected into seven normal subjects and twenty-eight genetically classified hyperlipidaemic patients to quantitate lipoprotein interconversion. The apoprotein B specific activity--time curves for VLDl and intermediate density lipoprotein (IDL, density = 1 . 006--1 . 019 g/ml) intersected at or before the IDL-B maximum in thirty-one studies (five normal controls and twenty-six hyperlipidaemic subjects) implying that all IDL-B may be derived from VLDL-B. The fractional conversion of VLDL-B to LDL-B (density 1 . 019--1 . 063 g/ml) following a simultaneous spike injection of 131I-VLDL and 125-LDL was obtained by deconvolution of the 125I and 131I-LDL-B activity curves. 21--65% (mean = 44%) of VLDL-B was converted to LDL-B in twenty-three subjects studied. The mean conversion time ranged from 10 to 24 h in ten normotriglyceridaemic subjects and from 19 to 42 h (mean = 33 h) in twelve hypertriglyceridaemic subjects. In one patient with broad-beta disease the mean conversion time was 55 h. LDL-B production from VLDL-B and total LDL-B synthetic rate were essentially equal in normal controls and normocholesterolaemic subjects and in the patient with broad-beta disease. But in all six patients with familial hypercholesterolaemia LDL-B synthetic rate significantly exceeded LDL-B production from VLDL-B, indicating direct secretion of 20--72% of LDL-B at a rate which correlates positively with plasma LDL concentration. Three of five patients with familial combined hyperlipidaemia showed a lesser but nevertheless significant direct secretion of LDL-B.
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PMID:Quantitative studies of very low density lipoprotein: conversion to low density lipoprotein in normal controls and primary hyperlipidaemic states and the role of direct secretion of low density lipoprotein in heterozygous familial hypercholesterolaemia. 678 Mar 63

Following ingestion of a fatty meal there is an increase in concentration of phospholipids and proteins in the plasma high density lipoproteins (HDL). To evaluate the resulting changes in HDL subclasses, the plasma HDL of six subjects were analyzed 4 to 8 h after ingestion of 100 ml of corn oil or 80 ml of corn oil with four eggs. Isopycnic density gradient ultracentrifugation of fasting plasma showed two broad components of HDL: a major peak of density (d) 1.11 to 1.17 g/ml (HDL3) and a smaller peak of d 1.07 to 1.11 g/ml (HDL2). Following ingestion of either type of fatty meal, there was an increase in lipoprotein mass in both peaks of HDL and their centers of mass were shifted to lower density (1.140 leads to 1.120 to 1.130 g/ml; 1.095 leads to 1.090 g/ml). Calculation of changes in HDL concentration (lipemic minus fasting) showed that the alterations in density gradient profile were due to a major increase in lipoproteins of d 1.102 to 1.137 g/ml, a smaller increase in a separate lipoprotein peak of 1.080 to 1.102 g/ml, and a small decrease in lipoproteins of d 1.137 to 1.165 g/ml. Redistribution of HDL mass into larger, less dense lipoproteins was also demonstrated by agarose gel chromatography or by minimal spin density gradient ultracentrifugation in a vertical rotor. The increase in mass of 1.080 to 1.102 lipoproteins was largely due to increased concentrations of phospholipid, cholesterol ester, and apoA-I, while the increase in 1.102 to 1.137 lipoproteins was due to increased concentrations of apoA-I, apoA-II, phospholipids, cholesterol, and cholesterol esters. Analytical ultracentrifugation of representative samples within these density intervals showed lipoprotein species with molecular weights and sedimentation coefficients, respectively, of 378,000, 5.8 (d 1.080 to 1.095); 248,000, 3.5 (d 1.110 to 1.120); and 173,000, 1.6 (d 1.135 to 1.150). Polyacrylamide gradient gel electrophoresis showed that the 1.080 to 1.102 lipoproteins contained a single lipoprotein band of diameter approximately 10.7 nm; the 1.102 to 1.137 lipoproteins contained a single band which varied in size fro 10.0 to 9.2 nm: and the 1.137 to 1.165 lipoproteins contained three species of diameters approximately 9.2, 8.8, and 8.2 nm. Within density intervals, the molecular weights, sedimentation coefficients, and diameters of the different lipoproteins were similar in fasting and lipemic plasma. Calculation of average molecular compositions shows that the major incremental HDL of d approximately 1.12 g/ml could be derived by addition of lipids to the largest species of fasting HDL3. Within density intervals, the particle contents of apoA-I and apoA-II were unchanged during lipemia, suggesting that apoprotein transfer causes interconversion of existing HDL species or formation of new particles with the same content of apoA-I and apoA-II as existing species.
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PMID:Changes in the distribution and composition of plasma high density lipoproteins after ingestion of fat. 679 85

Changes of plasma levels of apoproteins A-I, A-II and C-III were determined after oral and intravenous fat administration. The A-I levels increased in three out of four subjects after fat ingestion but no changes or even a slight decrease in the levels of A-I were observed after intravenous fat infusion. The A-II levels also increased after fat ingestion in two subjects but the levels either did not change or decreased slightly after fat infusion. The levels of C-III increased concomitantly with the increase of triglyceride levels after fat ingestion as well as fat infusion . After intravenous fat infusion, part of the C-III in the d greater 1.006 fraction shifted to the lighter fraction (d less than 1.006). These observations suggest that the increase in the levels of A-I and A-II after fat ingestion are a consequence of an increase in apoprotein synthesis in the intestine during fat absorption. The increase in the levels of C-III after fat ingestion as well as fat infusion seemed to be related to the capture of C-III inthe triglyceride rich particles, i.e. C-III accumulated in the circulation with triglyceride-rich particles. However, it appeared also to be possible that the rate of C-III synthesis increases during hyperlipidemia induced by fat infusion.
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PMID:Effects of oral and intravenous fat administration on the levels of apoproteins A-I, A-II and C-III in human. 680 12

In this review we have endeavored to emphasize the central role of the liver in normal lipoprotein metabolism and to demonstrate how derangements in these metabolic processes can lead to abnormalities characteristic of liver disease. Since changes in the concentration and composition of plasma lipids and lipoproteins occur frequently in liver disease, these findings may be useful in following the clinical course of patients with liver disease of various causes. It should be emphasized that elevated plasma triglycerides and cholesterol are due to underlying defects in lipoprotein metabolism and should not be confused with primary hyperlipidemia. Impaired cholesterol esterification, abnormal lipoprotein electrophoretic patterns and lipoprotein compositional changes, all reflect abnormalities of lipoprotein metabolism that are secondary to hepatocellular injury or cholestasis. These abnormalities are very sensitive indicators of fundamental metabolic defects that are related in part to LCAT and apoprotein activator deficiencies, impaired H-TGL and LPL activity and, perhaps, defective remnant lipoprotein clearance by the liver. Since these abnormalities tend to improve with clinical recovery they have proved to be reliable and sensitive indicators of hepatic function and thus, are useful in the assessment of liver disease.
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PMID:Lipoprotein metabolism in liver disease. 698 38

The apoproteins are the constitutive peptides of the plasma lipoproteins. The most widely employed nomenclature is that based on the family concept of constitutive polypeptides. The apoproteins are synthetized in the liver and/or in the intestine. During the lipolysis, apoprotein transfers and/or exchanges are observed. The apoproteins play a major role in the structure of the macromolecular lipid-protein complexes, and in the activity of several enzymes involved in the lipoprotein catabolism. An expanding information on apoprotein metabolism will allow a better comprehension of the hyperlipidemia pathogenesis.
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PMID:[Classification and metabolic relationship of plasma apoproteins (author's transl)]. 701 Feb 76


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