Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
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PMID:Post-heparin lipolytic activities and alterations of the chemical composition of high density lipoproteins in alcohol-induced type V hyperlipidemia. 649 35

Chronic renal disease with secondary hyperlipidemia is highly atherogenic. In uremia and patients on chronic hemodialysis there is a high incidence of atherosclerotic complications whereas the incidence of atherosclerotic disease is relatively low in the nephrotic syndrome. This is surprising, as nephrosis produces type-II hyperlipidemia, which is usually highly atherogenic. In this study 10 patients (5 male, 5 female) with a newly diagnosed nephrotic syndrome were compared to 10 controls (5 male, 5 female). As laboratory parameters, lipids, lipoproteins (VLDL, IDL, LDL, HDL2 and HDL3 by rate zonal centrifugation) and the percentage composition of the major apolipoproteins in VLDL, HDL2 and HDL3, as well as lipoprotein lipase (LPL), hepatic lipase (HTGL) and lecithin-cholesterol-acyl-transferase (LCAT) were measured. In nephrotic patients significantly higher plasma levels of cholesterol, triglycerides, phospholipids, VLDL, IDL and LDL were found, whereas HDL-chol, HDL2 and HDL3 were unchanged. LPL and HTGL were both significantly impaired, whereas LCAT was distinctly increased. The percentage composition of apolipoproteins in HDL2 and HDL3 was normal. In nephrotic VLDL, apo-AI was distinctly increased at the expense of a decrease in apo-CII, and increased LCAT was explained by the relative rise of apo-AI in nephrotic VLDL. The increase in apo-AI in VLDL is discussed as a possible reason for the low atherogenic risk of secondary hyperlipidemia in nephrotic syndrome.
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PMID:[Lipoproteins, apolipoproteins, lipoprotein lipase, hepatic triglyceride lipase and lecithin cholesterol acyltransferase in patients with nephrotic syndrome]. 661 72

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.
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PMID:Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet. 661 28

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

The effects of ethanol, acetaldehyde, acetate and lactate on lipoprotein lipase (LPL) activity and regulation have been investigated. None of the substances had any direct effect on the enzyme or enzyme-substrate complex. Ethanol and acetate interfered with LPL regulation studied in vitro using rat adipose tissue. Acetate administration to humans did not influence the activity of LPL and hepatic lipase in post-heparin plasma, nor was the intravenous fat tolerance test affected. Ethanol administration markedly increased and prolonged the hyperlipidemia induced by oral triglyceride intake; the effect of acetate was much less pronounced. Thus, acetate does not seem to interfere with LPL regulation in man. The previously described impairment in LPL activity and regulation after ethanol intake is probably mediated by ethanol itself.
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PMID:Acute effects of ethanol and its metabolites on plasma lipids and lipoprotein lipase activity. 688 18

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.
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PMID:The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients. 711 4

1. Significant positive correlations were found between the lipoprotein lipase and hepatic lipase activities of post-heparin plasma samples and plasma high-density-lipoprotein (HDL) cholesterol concentrations in 21 children with hyperlipidaemia and six normal adult males. 2. A significant positive correlation was also observed between the two lipase activities and the ratio of HDL cholesterol to apoprotein AI (apo AI) concentrations. 3. These findings provide further evidence that a significant proportion of HDL and possibly the HDL, subfraction is formed during the clearance of triglyceride-rich lipoproteins.
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PMID:Relationship between plasma high-density lipoprotein concentrations and lipoprotein lipase and hepatic lipase activities in children with hyperlipidaemia. 726 47

Cholesteryl ester storage disease (CESD) results from inherited deficiencies of the lysosomal hydrolase, acid lipase (LAL; E.C. 3.1.1.13). To establish the molecular defects in LAL deficiency, two unrelated probands with severely reduced LAL activity were examined. DNA amplification by reverse-transcription polymerase chain reaction and subsequent sequence analysis of LAL cDNA identified two mutant alleles. Patient 1, presenting with hepatosplenomegaly, mildly elevated liver function tests, and hyperlipidemia, was homozygous for a deletion of nucleotides 823 to 894 of the LAL cDNA. This 72-bp deletion maintained the reading frame and resulted in a loss of 24 amino acids from the LAL protein. Analysis of genomic DNA revealed that the 72 bp corresponded to an exon of the LAL gene. A single G to A point mutation at the last exon position was observed in the genomic DNA of patient 1, indicating a splicing defect with consecutive exon skipping underlying the 72-bp deletion. Patient 2 was a compound heterozygote for the 72-bp deletion and a dinucleotide deletion at positions 967 and 968. This deletion resulted in a shifted reading frame carboxyterminal of codon 296, and 43 random amino acids followed the frame shift. A premature stop at codon 339 truncated the mutant LAL protein by 34 amino acids. Allele-specific hybridization confirmed that patient 1 was homozygous for the 72-bp deletion mutation, and that patient 2 was a compound heterozygote for the 72-bp deletion and the 2-bp deletion.
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PMID:A 5' splice-region mutation and a dinucleotide deletion in the lysosomal acid lipase gene in two patients with cholesteryl ester storage disease. 775 11

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


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