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

The mechanism of hyperlipidaemia in the nephrotic syndrome has not been fully established. We propose that it results from hypoalbuminaemia due to inhibition of the reaction catalysed by lecithin cholesterol acyltransferase converting cholesterol of high density lipoproteins to cholesterol esters and to an inhibition of high density lipoprotein particle formation from very low density lipoproteins due to reduced activity of lipoprotein lipase.
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PMID:The mechanism of hyperlipidaemia in the nephrotic syndrome. 23 35

To clarify the mechanisms of hyperlipidemia caused by infusion of Intralipid 10%, we compared lipoprotein metabolism during intravenous Intralipid 10% and Intralipid 20%, which contains only half the amount of egg yolk lecithin for the same content of triglyceride as Intralipid 10%. Ten patients receiving 20 ml.kg-1.day-1 of Intralipid 10% and 10 receiving 10 ml.kg-1.day-1 of Intralipid 20% were fed exclusively by total parenteral nutrition (TPN) providing 1.1 g amino acid and 30 kcal.kg-1.day-1 for 4-6 wk. Intravenous Intralipid 10% caused a marked increase in low-density lipoprotein (LDL), together with increases in phospholipid and cholesterol, especially free cholesterol. The progressive increase in lipoprotein X was in proportion with that of LDL or total lipid, whereas no increase in lipids, LDL, or lipoprotein X was observed during intravenous Intralipid 20%. A significant increase in apolipoproteins CIII and E with Intralipid 10% also caused a rise in lipoprotein X. With Intralipid 20%, however, the alterations in apolipoproteins were not observed. Lecithin:cholesterol acyltransferase (LCAT) activity was significantly elevated with Intralipid 10 but not 20%. Disappearance of lipoprotein X after cessation of Intralipid 10% was relatively rapid, and the half-life was 24-60 h. From these findings, the hyperlipidemia with Intralipid 10% was caused almost exclusively by the increase in lipoprotein X. The excess lecithin may be responsible for the formation of and increase in lipoprotein X. Furthermore, it was revealed that Intralipid 20% could be safely used without inducing hyperlipidemia.
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PMID:Intravenous intralipid 10% vs. 20%, hyperlipidemia, and increase in lipoprotein X in humans. 152 30

The major plasma lipids, cholesterol and triglyceride, circulate in association with specific proteins as lipid-protein or lipoprotein complexes. The proteins direct and regulate the metabolism of these complexes in interacting with tissue enzymes and receptors. The metabolic fate of circulating triglyceride is governed by the activity of the enzyme lipoprotein lipase, situated in adipose tissue and skeletal muscle. Cellular demand for cholesterol, on the other hand, is met by activation of a specific receptor which mediates the delivery of sterol-rich lipoproteins to lysosomal degradation in liver and peripheral tissues. In order to prevent excess cholesterol accumulation at the periphery, there is a system of reverse cholesterol transport which involves assimilation and trapping of the sterol in the plasma lipoproteins through the action of the enzyme lecithin: cholesterol acyltransferase. Thereafter, the cholesterol is delivered to the liver, the only organ capable of excreting it in significant amounts. Disturbances in these processes may produce gross changes in the plasma lipid profile, clearly recognisable as hyperlipidaemia. However, it is becoming increasingly clear that a number of inherited traits can subtly perturb the lipoprotein spectrum and increase coronary risk even in subjects whose plasma lipoprotein profile would be considered normal.
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PMID:Lipoprotein metabolism: an overview. 159 Jun 43

The purpose of this study was to characterize the lipoprotein profile and cholesterol metabolism in Yoshida rats, a strain of inbred genetically hyperlipemic animals. For comparison, Brown Norway rats were used as control animals. Plasma cholesterol and triglycerides were higher in Yoshida as compared to Brown Norway, the elevation of cholesterol being due to a rise in HDL fraction. Triglyceride distribution among lipoproteins showed an increase in VLDL fraction. Hyperlipemia was not related to diabetes, hypothyroidism or nephropathy. Plasma triglycerides production was increased in Yoshida rats, while lipoprotein and hepatic lipases were similar in the two groups. Hypercholesterolemia was associated with a defect of lipoprotein receptor activity and with elevated HMG-CoA reductase and cholesterol 7 alpha - hydroxylase; conversely ACAT activity was lower in Yoshida as compared to Brown Norway rats. Sterol fecal excretion was comparable in the two groups and hypercholesterolemia in Yoshida rats was not associated to an increase of cholesterol saturation of the bile. We suggest that lipoprotein overproduction is the main cause for hyperlipidemia in this strain of rats.
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PMID:Plasma lipoproteins and cholesterol metabolism in Yoshida rats: an animal model of spontaneous hyperlipemia. 159 76

This study examined the preventive effects of green tea extract on hyperlipidemia and lipid accumulation in the liver and aorta of mice fed an atherogenic diet enriched with 1.5% cholesterol, 0.5% cholic acid and 5% linoleic acid for a period of 14 weeks. The animals were given green tea extract in drinking water at doses of 50, 100 and 200 mg/kg/day. Treatment with green tea extract prevented the increase of serum cholesterol induced by the atherogenic diet 6 weeks after the start of the experiment. The increase of serum lipid peroxides was markedly prevented in a dose-related manner. The green tea extract also tended to prevent the increase of serum phospholipid and the decline of lecithin: cholesterol acyltransferase, but could not prevent decreases in serum triglycerides and high-density lipoprotein cholesterol. As for liver cholesterol, its content, particularly free cholesterol, in mice fed the atherogenic diet could be prevented from increasing by treatment with the extract at 50 and 100 mg/kg/day. In addition, the increase of aortic cholesterol, particularly esterified cholesterol, could be prevented in a dose-related manner. These results suggest that green tea has anti-atherosclerotic activity.
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PMID:[Preventive effects of green tea extract on lipid abnormalities in serum, liver and aorta of mice fed a atherogenic diet]. 187 61

Hepatic, heparin-releaseable lipase is a multifunctional enzyme that may act on all lipoprotein classes present in plasma from fasted subjects. Recent evidence suggests that the enzyme also plays a role in the metabolism of chylomicronremnants. Its activity is impaired in normolipidemic patients with coronary heart disease, which also have a delayed removal of chylomicronremnants from plasma. Therefore hepatic lipase, in addition to lipoprotein lipase, plays an important role in postprandial lipoprotein metabolism. The activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesterylester transfer protein (CETP) are virtually unchanged after the ingestion of an oral fat load by normolipidemic subjects. However, the net mass transfer of cholesterylesters out of HDL into apo B-containing lipoproteins (chylomicronremnants, VLDL/IDL/LDL) is strongly increased. All triglyceride-rich lipoprotein fractions accumulate postprandially and, as a result of CETP action, become enriched in cholesterylesters. Defects in hepatic remnant removal may result in influx of remnants into the arterial wall. In patients with hyperlipidemia (and increased risk for atherosclerosis) the CETP-mediated formation of cholesterylester-rich remnants may operate, not only during the postprandial phase, but continuously.
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PMID:[Role of hepatic lipases, cholesterol ester transfer proteins and LCAT in the postprandial phase]. 208 75

1. Hyperlipidaemia is associated with diabetes mellitus. 2. A comparison of cholesterol synthesis and utilization in alloxan-induced diabetic rats and rabbits revealed that interspecies differences existed only in the response of the key enzymes regulating cholesterol utilization, namely cholesterol 7 alpha-hydroxylase and ACAT in the liver and intestine respectively. 3. The activity of cholesterol 7 alpha-hydroxylase was enhanced in diabetic rats but was markedly reduced in diabetic rabbits. 4. Intestinal ACAT activity, though unchanged in diabetic rats was reduced in diabetic rabbits. 5. Such species differences in cholesterol utilization may underlie the different degree of susceptibility to hypercholesterolaemia that exists between these two species.
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PMID:A comparative study of the rate-limiting enzymes of cholesterol synthesis, esterification and catabolism in the alloxan-induced diabetic rat and rabbit. 342 2

Lipoprotein classes isolated from the plasma of two patients with apolipoprotein AI (apo AI) and apolipoprotein CIII (apo CIII) deficiency were characterized and compared with those of healthy, age- and sex-matched controls. The plasma triglyceride values for patients 1 and 2 were 31 and 51 mg/dl, respectively, and their cholesterol values were 130 and 122 mg/dl, respectively; the patients, however, had no measurable high density lipoprotein (HDL)-cholesterol. Analytic ultracentrifugation showed that patients' S degrees f 0-20 lipoproteins possess a single peak with S degrees f rates of 7.4 and 7.6 for patients 1 and 2, respectively, which is similar to that of the controls. The concentration of low density lipoprotein (LDL) (S degrees f 0-12) particles, although within normal range (331 and 343 mg/dl for patients 1 and 2, respectively), was 35% greater than that of controls. Intermediate density lipoproteins (IDL) and very low density lipoproteins (VLDL) (S degrees f 20-400) were extremely low in the patients. HDL in the patients had a calculated mass of 15.4 and 11.8 mg/dl for patients 1 and 2, respectively. No HDL could be detected by analytic ultracentrifugation, but polyacrylamide gradient gel electrophoresis (gge) revealed that patients possessed two major HDL subclasses: (HDL2b)gge at 11.0 nm and (HDL3b)gge at 7.8 nm. The major peak in the controls, (HDL3a)gge, was lacking in the patients. Gradient gel analysis of LDL indicated that patients' LDL possessed two peaks: a major one at 27 nm and a minor one at 26 nm. The electron microscopic structure of patients' lipoprotein fractions was indistinguishable from controls. Patients' HDL were spherical and contained a cholesteryl ester core, which suggests that lecithin/cholesterol acyltransferase was functional in the absence of apo AI. The effects of postprandial lipemia (100-g fat meal) were studied in patient 1. The major changes were the appearance of a 33-nm particle in the LDL density region of 1.036-1.041 g/ml and the presence of discoidal particles (12% of total particles) in the HDL region. The latter suggests that transformation of discs to spheres may be delayed in the patient. The simultaneous deficiency of apo AI and apo CIII suggests a dual defect in lipoprotein metabolism: one in triglyceride-rich lipoproteins and the other in HDL. The absence of apo CIII may result in accelerated catabolism of triglyceride-rich particles and an increased rate of LDL formation. Additionally, absence of apo CIII would favor rapid uptake of apo E-containing remnants by liver and peripheral cells. Excess cellular cholesterol would not be removed by the reverse cholesterol transport mechanism since HDL levels are exceedingly low and thus premature atherosclerosis occurs.
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PMID:Familial apolipoprotein AI and apolipoprotein CIII deficiency. Subclass distribution, composition, and morphology of lipoproteins in a disorder associated with premature atherosclerosis. 650 64

Several enzyme activities involved in lipid hydrolysis (acid and neutral cholesterol esterase and lipase) or synthesis (acyl-CoA synthetase, acyl-CoA: cholesterol acyltransferase and cholinephosphotransferase) were assayed in the aortas of rats with nephrosis induced by daunomycin and of rats fed on high cholesterol diet. In nephrotic rats activities of some enzymes involved in lipid hydrolysis, but not in synthesis, were increased. On the contrary, in rats fed on high cholesterol diet, the activities of all enzymes involved in lipid synthesis were significantly increased, with some increase in those involved in lipid hydrolysis. In nephrotic rats fed on high cholesterol diet all enzyme activities were markedly increased. From the view point of accumulation of cholesterol ester (CE), the ratio of hydrolysis of CE in lysosomes to CE incorporated from the blood and the ratio of hydrolysis of CE to reesterification of free cholesterol in microsomes were considered to be important. From this point of view, nephrotic hyperlipidemia was not so atherogenic as hyperlipidemia induced by the diet. The role of serum high density lipoproteins in lipid metabolism in the aorta was discussed.
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PMID:Lipid metabolism in the aorta of daunomycin-induced nephrotic rats. 664 60

Weanling Wistar rats were pair-fed for 8 days control and magnesium-deficient diets. Acute magnesium deficiency increased plasma triglycerides and free cholesterol levels and decreased esterified cholesterol levels. The plasma activity of lecithin--cholesterol acyltransferase was markedly diminished in fasting magnesium-deficient rats (54% reduction) and plasma high density lipoprotein (HDL) free cholesterol was significantly increased in the HDL fraction. The results of this study showing that dietary magnesium affects the activity of the enzyme involved in the esterification of free cholesterol to cholesterol ester provide a possible basis for the reduced plasma cholesterol esterification and hyperlipidemia associated with acute magnesium deficiency.
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PMID:Reduction of plasma lecithin--cholesterol acyltransferase activity by acute magnesium deficiency in the rat. 674 30


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