Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyslipidemia may contribute to atherosclerosis in hemodialysis patients. While hypertriglyceridemia is relatively common in this population, hypercholesterolemia is not. Since abnormalities in various plasma cholesterol fractions and lipoproteins have been associated with an increased incidence of cardiovascular disease in the nonuremic population, we examined these abnormalities to determine whether they occur in patients with chronic renal failure. Twenty-four patients on maintenance hemodialysis were studied. We found that, despite relatively low plasma total cholesterol levels, a substantial number of patients had low high-density lipoprotein cholesterol, low apolipoprotein AI, and high apolipoprotein B levels. Furthermore, approximately 40% and 30%, respectively, of the patients had elevated plasma levels of lipoprotein(a) and remnants of chylomicron and very low-density lipoprotein. Lipoprotein(a) levels could not be predicted from any of the variables that were studied. The abnormal plasma levels of these potentially atherogenic lipids and lipoproteins suggest that they may contribute to the high incidence of cardiovascular diseases in the hemodialysis population.
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PMID:Atherogenic lipids and lipoproteins in hemodialysis patients. 835 53

Dyslipidemia is an important risk factor for atherosclerotic vascular disease. Serum lipoprotein (a) [Lp(a)] has been implicated as an independent atherogenic risk factor. We measured serum (Lp(a) levels in our patients and studied its correlations with other lipoproteins and clinical parameters. All stable patients on continuous ambulatory peritoneal dialysis (CAPD) for more than one month were enrolled in the study. Fasting serum Lp(a), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apolipoprotein-A and apolipoprotein-B levels were measured on entering the CAPD program and at 3 monthly intervals. One hundred and nine patients (M/F: 65/44, mean age +/- SD: 59.5 +/- 12.0 years) were studied. Fifty-two patients had diabetes mellitus. Age- and sex-matched normals were used as controls. Serum Lp(a) levels were raised in 54.5% of CAPD patients compared to 18.6% of controls (p < 0.01). There was no significant change in Lp(a) levels over time. Serum Lp(a) levels showed positive and negative correlations with LDL-cholesterol and triglycerides, respectively, but not with age, sex, diabetic status, and serum total cholesterol and albumin levels. Thirty-six of 54 (66.7%) patients with serum Lp(a) levels greater than 30 mg/dL had either coronary, cerebral, and/or peripheral vascular disease compared to 30/55 (54.5%) of patients with serum Lp(a) levels less than 30 mg/dL (p = NS). In conclusion, serum Lp(a) levels were raised in a significant proportion of CAPD patients, but there was no significant association with vascular disease.
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PMID:Lipoprotein (a) levels and clinical correlations in CAPD patients. 853 86

Renal disease is accompanied by specific alterations of the lipoprotein metabolism. While marked hyperlipidemia is a characteristic finding in the nephrotic syndrome, the dyslipoproteinemia of renal insufficiency is predominantly reflected in an abnormal apolipoprotein pattern but does not necessarily include elevated plasma lipid concentrations. The specific changes in nephrotic syndrome include increased formation primarily of cholesterol-rich and to a varying extent of triglyceride-rich ApoB-containing lipoproteins in the VLDL-LDL density range with little or no change among the ApoA-containing lipoproteins in HDL. The dyslipoproteinemia of renal failure is, on the other hand, mainly characterized by a decreased catabolism of the triglyceride-rich ApoB-containing lipoproteins with increased concentrations of partially metabolized lipoproteins of intermediate and very low density and a decreased concentration of ApoA-containing lipoproteins in HDL. In addition, increased levels of Lp(a) are found both in the nephrotic syndrome and in renal failure. Dialysis treatment appears to have only a modest influence on the renal dyslipoproteinemia. Due to its atherogenic character, the dyslipidemia of renal disease may be related to the accelerated development of cardiovascular disease in these patients.
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PMID:Diagnosis and classification of dyslipidemia in renal disease. 871 66

In the process of screening apolipoprotein (apo) E genotypes in a population of subjects with lipid abnormalities, we have identified five subjects (one homozygote and four heterozygotes) with an abnormal 109 base pairs band following apo E restriction isotyping of amplified DNA with the restriction endonuclease CfoI. The polymerase chain reaction (PCR) products were cloned and their sequencing revealed a C-->A substitution at the first nucleotide of codon 136. This mutation resulted in an amino acid substitution Arg to Ser, previously described as apo E2 Christchurch. Family studies were carried out for four of the probands. In these kindreds, stepwise multiple regression analyses indicated that 78% of the cholesterol variability in men was predicted by body mass index, age and the rare apo E2 (Arg136-->Ser) variant. In women, age and the apo E2 (Arg136-->Ser variant predicted 54.9% of the variability in cholesterol levels. Linkage analysis suggested that the presence of the apo E2 (Arg136-->Ser) variant was linked with the occurrence of cholesterol enriched triglyceride rich lipoproteins and with an incomplete dominance of type III hyperlipoproteinemia. Our data indicates that this mutation may be a relatively common cause of dyslipidemia in the Spanish population.
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PMID:Incomplete dominance of type III hyperlipoproteinemia is associated with the rare apolipoprotein E2 (Arg136-->Ser) variant in multigenerational pedigree studies. 872 10

The review examines the evidence that the supply of cholesterol available for incorporation into nascent lipoprotein particles exerts a regulatory influence on apolipoprotein (apo) B secretion by the liver. Support for this hypothesis comes both from in vitro experiments and from recent observations in normal subjects and patients with dyslipidemia associated with familial hypercholesterolemia, obesity, noninsulin dependent diabetes mellitus, growth hormone deficiency and cholesteryl ester storage disease. The findings do not negate a role for triglyceride synthesis in determining apoB secretion in very low density lipoprotein, but the inhibitory effects on the latter process of pharmacological blockade of cholesterol synthesis or esterification suggest that it is conditional upon an adequate supply of cholesteryl ester.
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PMID:Role of cholesterol in regulating apolipoprotein B secretion by the liver. 872 9

In accordance with the principles of protein biochemistry, apolipoprotein is the only protein which: 1) forms a protein-lipid complex (PLC) mainly from one class of lipids; 2) determines its functional role; 3) causes dyslipidemia in the genetic destruction of apoproteins or their quantitative ratio. Blood flow lipid transport is based on the functional specificity of their apoproteins; each apoprotein forms a functionally independent PLC; each PLC is formed from one class of lipids; each PLC has one protein-vector; each protein-vector interacts only with receptor. The basis of a united cycle functioning in lipid transport is the difference of primary apoprotein structure. Cholesterol performs an auxiliary function in triglyceride transport by providing circulation in the functional cycle. Lipid transport in blood flow is based, first, on the principles of protein biochemistry and, second, on those of lipidology.
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PMID:[Blood flow lipid transport from viewpoint of protein biochemistry]. 898 7

Low-density lipoprotein (LDL) particles are heterogeneous in density, size, and chemical composition, and this heterogeneity is thought to be genetically influenced. In the present study, plasma LDL subclasses in 248 children aged 7 to 13 years were analyzed by gradient gel electrophoresis. The prevalence of small dense LDL (SDLDL), a potent atherogenic LDL, was 9.3%, which is lower than that reported in adults. Furthermore, children with this LDL subclass showed increased body fatness and dyslipidemia, including elevated plasma triglyceride and apolipoprotein (apo) B concentrations and decreased plasma high-density lipoprotein (HDL) cholesterol and apo A-I concentrations, compared with children without this phenotype. These findings suggest that in addition to genetic factors, environmental factors that affect these cardiovascular risk factors may also influence expression of the SDLDL subclass.
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PMID:Characterization of low-density lipoprotein subclasses in children. 903 Aug 19

To determine whether enhanced activity of cholesteryl ester transfer protein (CETP) contributes to the development of atherogenic lipoprotein profiles in obese children, plasma CETP activity was assayed according to a micro-method, by co-incubating lipoprotein-deficient samples with exogenous donor and acceptor lipoproteins. The study subjects were 31 obese children (14 males and 17 females). Serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), TC:high-density lipoprotein (HDL)-C, LDL-C:HDL-C, apolipoprotein (apo) B, and apo B:apo Al were increased in obese children. Thus they appeared to exhibit an atherogenic lipoprotein profile, with a relative decrease in cholesterol carried by HDL compared with the cholesterol in the other lipoprotein fractions. The mean fasting plasma insulin level was also increased. CETP activity was significantly higher in the obese children than in nonobese control children, and was correlated with LDL-C, TC:HDL-C, LDL-C:HDL-C, and apo B:apo Al. These results suggest that an increase in plasma CETP activity results in atherogenic change in lipoprotein metabolism in obese children. The increase in CETP may be due to the adiposity or insulin resistance. Alternatively, dyslipidemia per se, physical inactivity or excessive fat intake, that are commonly found in obese children, may contribute to the increase in CETP activity.
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PMID:Increased plasma cholesteryl ester transfer activity in obese children. 906 17

Lipid abnormalities are major risk factors for premature coronary artery disease (CAD). However, the type and prevalence of dyslipidemia in these patients have not been well characterised, especially in some ethnic groups. The purpose of the present work was to determine the lipid disorders in patients of Northwestern Greece with premature CAD. The study population comprised of 132 men and 38 women who underwent elective diagnostic arteriography in our University Hospital. Subjects with > or = 1 lesion that narrowed the lumen of any of the 15 coronary artery segments by > or = 70% were considered to be CAD cases (n=108), whereas those with narrowing < 70% were excluded (n=54). Asymptomatic subjects (n=104) matched for age and sex were taken as controls. Compared with the controls, patients with premature CAD had increased serum levels of total cholesterol, LDL cholesterol, triglycerides, Apo B, and Lp(a), and decreased serum levels of HDL cholesterol and Apo A1. A lipoprotein or apolipoprotein abnormality was identified in 89 CAD patients (82.4%). The increased serum Apo B level (> 130 mg/dl) was the most common lipid abnormality observed in 72 patients. However, the most prevalent dyslipidemic phenotypes in our patients were type IIA followed by hypoalpha and hyperApoB. Compared to the control population, CAD patients had increased incidence of IIA and hypoalpha phenotypes. On the contrary, a normal lipoprotein phenotype was more common in the control population compared to CAD patients (56.7% vs. 17.6%, P<0.001). We conclude that the majority of Greek patients with premature CAD exhibit lipid and lipoprotein abnormalities, which to a large extent can be defined by determining the traditional lipid parameters (total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides). However, in some cases the value of the quantification of other lipid parameters such as apolipoproteins and Lp(a) should be taken into account.
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PMID:Lipid abnormalities in Greek patients with coronary artery disease. 915 72

One hundred forty-seven relatives of 43 patients with "classical" type III hyperlipoproteinemia (HLP) having the apolipoprotein (apo) E2/2 phenotype were studied to determine the occurrence of hyperlipidemia and the presence of further possible genes for lipoprotein disorders in these families. In 12 pedigrees primary dyslipidemia was prevalent among patients and respective blood-relatives. In these kindreds the coexistent presence of genes for familial combined hyperlipidemia (n = 6), familial hypertriglyceridemia (n = 5), and familial hypercholesterolemia (n = 1), respectively, was supposed. Our results, therefore, confirm and extend previous data on the multifactorial genesis of the diseases. Besides homozygosity for a receptor binding-defective isoform of apo E (apo E2), additional genes for familial lipoprotein disorders might operate in the pathogenesis of type III HLP. This is the largest family study performed so far in this primary lipoprotein disorder.
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PMID:Genetics of type III hyperlipoproteinemia. 918 57


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