UMLS:C0020473 - FACTA Search

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

The results of plasma lipid and lipoprotein analysis in two related patients, brother (R.U.) and sister (R.R.) with analbuminemia, and three first-degree relatives (parents and sister) are reported. Both patients showed a remarkable increase in cholesterol and phospholipid levels, and there was a corresponding increase in serum apo B and apo A-I. This hyperlipidemia is due to a selective increase in LDL and HDL concentrations. R.U. showed an increase in both HDL2- and HDL3-cholesterol, R.R. only in HDL3-cholesterol. VLDL concentration was reduced in R.U. and normal in R.R. The plasma lipoprotein electrophoretic pattern did not correspond to any of the phenotypes in Fredrickson's classification. Composition of the different lipoprotein fractions was normal in the patients and family members. Serum FFA level in R.R. was very low. An increase in the plasma protein fractions, particularly the transport fractions, was confirmed in both patients. The possible pathophysiology of the hypercholesterolemia in these patients is discussed. Unlike other reported cases, clinical signs of atherosclerotic complications were absent.
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PMID:Characterization of hyperlipidemia in two patients with analbuminemia. 685 Nov 39

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43

The present investigation was designed to examine the influence of genetic Type IV hyperlipoproteinemia on the metabolism of lipids in response to estrogen exposure. The influence of 17-Beta-estradiol * was examined in a dose-response study over a range of hormone concentration from 10 to 100 pg/ml in genetic hyperlipidemic Zucker rats. In oophorectomized female rats, replacement levels of plasma estradiol of 40 pg/ml resulted in maximal hypertriglyceridemia of approximately 500 mg/dl representing a 5-fold exaggeration of that observed in control genetically norm-lipemic animals. This hypertriglyceridemia was associated with an increased production of triglyceride (TG) in excess of clearance, with a resulting production: clearance ratio of approximately 1.5. Exposure to maximum blood levels of estradiol, approximately 100 pg/ml, resulted in sub-normal levels of plasma TG (-145 mg/dl) in association with a reduced production: clearance ratio of approximately 0.36. In contrast to the marked hypocholesterolemic response to maximum estrogen exposure seen in normolipemic animals, the genetic Type IV hyperlipemic animal failed to demonstrate reduced plasma cholesterol concentration. This phenomenon was related to a rise in plasma LDL concentration in conjunction with parallel reduction in plasma HDL2 levels.Thus, an abnormal ratio of excessive LDL: HDl emerged in response to estrogen exposure in this model of human Type IV lipemia. This observation suggests that the genetic predisposition of the host may be critical to both the quantitative as well as the qualitative response to estrogen.
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PMID:Influence of genetic hyperlipemia in the Zucker rat upon the lipemic response to graded estradiol exposure. 707 97

Individual and pooled samples of plasma from normolipemic and hyperlipemic subjects were separated into very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein fractions (HDL2 and HDL3) by conventional ultracentrifugation and total lipid extracts prepared by standard methods. The composition of the molecular species of the sphingomyelins in each lipoprotein class was determined by packed column and capillary gas-liquid chromatography of the trimethylsilyl (TMS) and t-butyldimethylsilyl (t-BDMS) ethers and by gas chromatography - mass spectrometry of t-BDMS ethers of ceramides derived by phospholipase C hydrolysis of the corresponding parent compounds. It was demonstrated that the molecular weight of the species of the sphingomyelins increases with the density of the lipoprotein fraction in normolipemic subjects, and that this increase is due to an increase in the chain length of the fatty acids in the ceramide molecules. In contrast, patients with type IV hyperlipoproteinemia possessed similar species in the LDL and HDL fractions, while maintaining normal differences between HDL and VLDL. Type III patients possessed normal HDL and VLDL differences, but had variable LDL. Type II patients had ceramide profiles for VLDL, LDL, and HDL fractions that were very similar to those of normals. The differential distribution of the molecular species of the sphingomyelins is rationalized on the basis of a lateral phase separation of the short and long chain sphingomyelins during the shedding of the excess VLDL or chylomicron surface material and a subsequent preferential transformation of the long chain species into HDL. The LDL sphingomyelins in type III hyperlipemia are variable and approximate either the VLDL or HDL composition.
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PMID:Differential distribution of sphingomyelins among plasma lipoprotein classes. 729 45

Lipoprotein and liver lipids of spontaneously hyperlipidemic Yoshida rats were compared with those of normolipidemic Wistar animals for studying their age- and strain-related differences. Both strains showed an age-related increase in the total plasma cholesterol concentration. However, the Yoshida strain had a higher content of cholesteryl esters and triglycerides than the Wistar strain in both young and adult animals (2- and 8-month-old animals, respectively). The free cholesterol content was also higher, but only in the 8-month-old animals. Both strains showed an age-related increase in the proportion of HDL1 and a symmetrical decrease in both the HDL2 and HDL3 subfractions, but the variations were more evident in the Yoshida strain. The study of strain-related differences suggested that the spontaneous hypertriglyceridemia of the Yoshida strain was not only related to the higher amount and proportion of the VLDL fraction, but also to the higher content of triglycerides in the LDL fraction. The livers of Yoshida rats accumulated more triglycerides (with an age-related progression) than those of Wistar rats. The major lipid classes in the liver of Yoshida rats contained a significantly higher proportion of monounsaturated fatty acyls. Furthermore, this proportion showed an age-related increase in all the lipid classes, but in cholesteryl esters. This suggested that liver desaturases had a relevant role in the development of hyperlipidemia, and of its age-related variations, in the Yoshida strain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related variations in plasma and liver lipids of Yoshida rats: a comparison with Wistar rats. 759 92

The accelerated atherosclerosis in diseases associated with elevated remnant lipoprotein levels has directed interest toward the response of this lipoprotein species to lipid-lowering treatment. The effect of fluvastatin--a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor--was compared with that of placebo on parameters of remnant metabolism in 57 patients with moderate hypercholesterolemia, but not heterozygous familial hypercholesterolemia, type III hyperlipidemia, or endogenous hypertriglyceridemia. Fluvastatin therapy resulted in decreases versus baseline in plasma total cholesterol, low density lipoprotein cholesterol (LDL-C) and LDL apolipoprotein (apo) B levels of 18%, 20%, and 18%, respectively (p < 0.01). Plasma parameters related to remnant metabolism were also significantly decreased: intermediate density lipoprotein by 43% and apo E by 22% (p < 0.01). The percent decrease in plasma intermediate density lipoprotein cholesterol level was twice that of LDL-C and 50% greater than the decrease seen in very low density lipoprotein cholesterol (VLDL-C), which was decreased by 28%. Total triglycerides were reduced by 11% and VLDL apo B by 24%, whereas high density lipoprotein cholesterol (HDL-C) rose significantly by 8%, HDL2-C by 24%, and HDL3-C by 3%. There were no increases in apo A-I levels compared with placebo nor any significant change in plasma lipoprotein(a) levels. The composition of LDL and VLDL particles did not appear to be altered by therapy, as assessed by the LDL-C:LDL-B, VLDL-C:VLDL-B, or triglyceride:VLDL-B ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. 760 88

This study was designed to evaluate the therapeutic effectiveness of 3 different pharmacologic lipid-lowering regimens in the treatment of patients with clustered lipid risk factors. Sixty-five patients with low high-density lipoprotein (HDL) levels and hypertriglyceridemia were randomized to 1 of 3 treatment arms: pravastatin/niacin, pravastatin/magnesium, or pravastatin/placebo. After 18 weeks, patients in the pravastatin/niacin group had a -41% change in the total cholesterol/HDL ratio compared with -13% in the pravastatin/magnesium arm and -16% in the pravastatin/placebo group. The HDL2 and HDL3 subfractions, as well as the apolipoprotein A-I levels, were increased significantly only in the pravastatin/niacin arm. The levels of small dense low-density lipoprotein (LDL) cholesterol (LDL3) were decreased to a greater extent in the pravastatin/niacin arm (-43%) than in either the pravastatin/magnesium (-13%) or the pravastatin/placebo (-20%) arm. Only the pravastatin/niacin regimen significantly diminished postprandial lipemia (-32% change in the remnant particle triglyceride concentration and decreased very-low-density lipoprotein remnant levels). Thus, in this group of patients with clustered risk factors, the combination of pravastatin and niacin resulted in significant improvements in HDL and triglyceride levels, total cholesterol to HDL ratio, small dense LDL levels, and postprandial lipemia. Pravastatin alone or in combination with magnesium resulted in less significant changes that were largely limited to LDL cholesterol reduction.
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PMID:Effects of pravastatin with niacin or magnesium on lipid levels and postprandial lipemia. 765 48

The behavior of apolipoprotein-defined subpopulations LpAI and LpAI,AII within high density lipoprotein (HDL) subclasses 2 and 3 was analyzed in the postprandial phase after a fat load. For the whole group of subjects, increases in plasma concentrations of HDL, principally due to the influx of lipoprotein surface components, were largely confined to the HDL3 density range and involved LpAI,AII and LpAI. However, the degree of postprandial lipemia influenced the distribution of surface remnants between the subfractions. In subjects with a limited postprandial rise in triglycerides, increased HDL mass was predominantly associated with LpAI,AII, and equally distributed between HDL2 and HDL3. Conversely, subjects with exaggerated postprandial lipemia manifested increased mass primarily within the HDL3 density range, implicating both LpAI,AII and LpAI. Stepwise regression analysis identified a two-variable model, involving LpAI,AII within HDL2 and LpAI within HDL3, as best defining the relationship between postprandial lipemia and the increase in HDL mass. Postprandial increases in triglyceride content were observed for all HDL subfractions, whilst modifications to the core lipid mass ratios were significant only for LpAI,AII. Stepwise regression analysis revealed a significant correlation between postprandial lipemia and the increase in triglyceride concentration only of LpAI,AII within HDL3. The results suggest that postprandial lipemia differentially influences apolipoprotein-defined HDL subfractions. The extent of postprandial lipemia may determine the involvement of different HDL subfractions in postprandial lipoprotein metabolism.
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PMID:Postprandial lipemia differentially influences high density lipoprotein subpopulations LpAI and LpAI,AII. 780 72

There is a general interest to know whether lipoprotein(a) [Lp(a)] is under hormonal control. Hypothyroidism is a well known cause of secondary hyperlipidemia, which mainly affects low density lipoprotein (LDL) cholesterol levels, but the result on the effects of L-T4 replacement therapy on the Lp(a) concentration is controversial. We studied 12 severely hypothyroid, hypercholesterolemic patients under basal conditions and during L-T4 treatment. We found a rapid decrease in both LDL cholesterol (5.71 +/- 0.62 vs. 4.37 +/- 0.44 mmol/L basally and after 1 month of thyroid replacement, respectively) and apolipoprotein-B (Apo-B) levels (1.89 +/- 0.02 vs. 1.52 +/- 0.17 g/L, respectively); these changes persisted for up 1 yr of analytical euthyroidism and paralleled the improvement in the thyroid status of the patients. In contrast, the plasma Lp(a) concentration did not change at any time (496 +/- 123, 464 +/- 128, and 441 +/- 110 mg/L under basal conditions and after 1 and 14-15 months of thyroid replacement, respectively), and the small fluctuations observed in some patients did not correlate with those in LDL cholesterol or Apo-B, and were not associated with any particular Apo(a) phenotype. In relation to HDL fractions, high density lipoprotein3 (HDL3) remained stable, but HDL2 cholesterol and phospholipid levels decreased during treatment, changes that were the inverse of those in postheparin plasma hepatic lipase activity. Patients in the present study were normotriglyceridemic, except one who was hypertriglyceridemic at diagnosis, but even in this patient, triglyceride levels were unaffected by T4 substitution therapy, as was postheparin plasma lipoprotein lipase activity. The changes observed in LDL, HDL2, and hepatic lipase activity delineate the lipoprotein-related response to T4 replacement therapy, whereas potential individual fluctuations in Lp(a) levels are probably more dependent on other factors, such as the production rate, which are not affected by thyroid hormones.
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PMID:Long-term thyroid replacement therapy and levels of lipoprotein(a) and other lipoproteins. 785 21

The purpose of this study was to examine the influence of brisk walking on postprandial lipemia in 26 sedentary women aged 41 to 55 years. The lipemic response to a high-fat meal (mean +/- SEM: 73.8 +/- 1.3 g fat, 66% energy; 81.8 +/- 1.4 g carbohydrate) was determined pretraining and posttraining. Blood samples were obtained in the fasted state and hourly for 6 hours after the meal. Serum was analyzed for triacylglycerol (TAG), total cholesterol, high-density lipoprotein (HDL) and HDL2 cholesterol, apolipoproteins (apos) A-I and B, nonesterified fatty acids (NEFA), glucose, and insulin. Subjects were randomly assigned to one of two groups: walkers (n = 13) followed a program of brisk walking (average of 21 +/- 1 [range, 17 to 27] min.d-1 at 1.76 +/- 0.02 m.s-1), whereas controls (n = 13) maintained their habitual life-style. Procedures were repeated 12 weeks later, with 48 hours between the last training session and determination of postprandial lipemia. Eleven walkers and 13 controls completed the study. Responses over time were compared between groups (Mann-Whitney U, P < .05). Brisk walking improved endurance fitness and decreased body fatness, but had no influence on peak TAG concentration (walkers, 1.6 +/- 0.2 v 1.6 +/- 0.2 mmol.L-1; controls, 1.9 +/- 0.3 v 2.1 +/- 0.3) or the area under the TAG/time curve after the test meal. The area under the insulin/time curve decreased in walkers relative to controls. These results suggest that in sedentary women aged 41 to 55, brisk walking attenuates the serum insulin response, but not the lipemic response, to consumption of a high-fat mixed meal when these responses are determined 48 hours after the last exercise bout.
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PMID:Influence of 12 weeks of training by brisk walking on postprandial lipemia and insulinemia in sedentary middle-aged women. 788 87

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