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)

During a transverse survey, 3 groups of men with the same weight and age were compared. Group I included 42 patients with coronary disease documented by coronarography, group 2 included 19 subjects with normal coronary angiograms, and group 3 included 27 healthy controls who had not undergone coronarography. Subjects presenting diabetes or any factor associated with secondary dyslipidemia or able to modify lipid levels were excluded from study. The following parameters were measured: total cholesterol (Chol), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apoprotein A1 (apoA1), apoprotein B (apoB), lipoprotein (a) or Lp(a), fibrinogen, insulinemia and plasminogen activator inhibitor activity (PAI). The levels of chol, LDL-C and ApoB were the same in the 3 groups. The levels of TG, HDL-C, apoA1 and the ApoA-1/APoB ratio were significantly different between groups 1 and 2, on the one hand, and groups 1 and 3, on the other hand. The levels of Lp(a) and insulin were similar in the 3 groups. Fibrinogen levels were slightly higher in group 1 than in group 3. There was no significant difference between groups 1 and 2 with regard to any of the parameters. Subjects with angiographically normal coronary arteries and subjects with documented coronary disease exhibited similar lipid abnormalities. In this study, TG, HDL-chol, apoA1 and the apoB ratio were better predictors of cardiovascular risk than Chol, LDL-C or apoB.
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PMID:[Lipid indicators of vascular risk. A cross-sectional study of a group of coronary patients, a group of subjects with normal coronary angiography and a control group]. 156 63

Dyslipidemia is a major risk factor for atherosclerosis in adults and children. This study investigated the levels of lipoproteins in a northern Italian pediatric population, in relation to nutritional and familial factors. We studied 650 children on the basis of a 3-day dietary record; 361 of these children had their lipid levels [total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglycerides] measured by a dry, multilayer method and apoprotein A-I and B by an immunonephelometric method. Familial history of cardiovascular disease and dyslipidemia was recorded. Anthropometric variables were taken for each child. Mean TC and low-density lipoprotein cholesterol (LDL-C) were high compared with southern Italian data, but similar to those of other Western countries. Family history of cardiovascular disease could not identify children with higher levels of atherogenic lipoprotein. Nutritional factors affected lipoprotein levels. The most important finding was a higher TC/HDL-C ratio in the lower quartile of polyunsaturated fatty acid intake. Obese children had higher levels of ApoB, triglycerides, TC and LDL-C, and lower levels of HDL-C; figures were higher for obese boys than for obese girls. Our study confirms a high prevalence of elevated levels of atherogenic lipoproteins among the northern Italian pediatric population and an association with nutritional factors and weight.
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PMID:Cholesterol and lipoprotein levels in Milanese children: relation to nutritional and familial factors. 161 95

Atherosclerosis is the main cause of mortality in diabetic patients, and the incidence of coronary heart disease is increased in the presence of microalbuminuria. The mechanisms of this association are not known and could involve genetic factors (predisposition to hypertension), renal disease and dyslipidemia. An increase in plasma triglyceride and apoprotein B levels, a decrease in plasma HDL cholesterol, qualitative abnormalities of VLDL and HDL are related to cardiovascular risk in diabetic patients. All these factors are worsened by nephropathy. Lipoproteins abnormalities could be involved in the progression of renal injury. In microalbuminuric patients, it seems important to reduce glomerular hyperfiltration and to normalize glycemia and blood pressure in order to prevent impairment of renal injury and dyslipidemia induced by nephropathy. Early treatment of lipoprotein abnormalities could decrease the incidence of cardiovascular complications.
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PMID:[Association of atherosclerosis and nephropathy in diabetes mellitus. Role of lipid anomalies]. 183 72

In agreement with the protein biochemistry principles apolipoprotein is considered to the only protein which: 1) forms protein-lipid complex (PLC) based on one lipid grade; 2) determines its functional significance; 3) causes the development of dyslipidemia at genetic disorder of quantitative and qualitative protein composition. The lipid transport in blood flow is based on high functional specifics of each of apoproteins; each apoprotein forms functionally separate PLC; each PLC has got one protein-vector; each protein-vector interacts with only one receptor. The basis of united cycle functioning in lipid transport is the difference of primary apoprotein structure. Cholesterol conducts an auxiliary function in triglyceride transport providing circulation in functional cycle. The lipid transport in blood flow is based first of all on protein chemistry principles and secondary--on lipidology principles.
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PMID:[Lipid transport in blood from the protein chemistry viewpoint]. 748 72

Epidemiological studies have elucidated that diabetes mellitus (DM) is one of the risk factors of coronary heart disease and that DM often accompanies dyslipidemia. Dyslipidemia in DM can be classified as either quantitative or qualitative. Although dyslipdemia in DM is affected by the type of DM and glycemic conditions, the characteristics of dyslipidemia in DM, especially in NIDDM are the increase in triglycerides accompanied by the decrease in HDL-cholesterol level. Recently, new commercial kits for measurement of atherogenic lipoproteins which increase in DM are clinically available. The usefulness of these kits in DM was reviewed. Polyacrylamide electrophoresis can detect IDL and Lp(a) qualitatively. It has also become possible to estimate Lp(a) quantitatively by ELISA, TIA and LIA methods. Remnant lipoprotein can be measured in the fraction unbound to anti-apo A1 and anti-apo B100 antibodies by immunoaffinity gel analysis. Apoproteins, apoprotein E phenotype, post-heparin lipoprotein lipase, and Lp AI (HDL with apo AI and without apo AII) can be measured by the commercially available kits. Modified LDLs (glycated, oxidative) increase in DM, but their measurements remain complicated at the moment. Analysis of plasma fatty acids by gaschromatography is useful for dietary assessment. The measurement of these new markers seems to be useful to assess the extent of atherogenic risk in DM.
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PMID:[Plasma fatty acids, lipids, lipoprotein and macroangiopathy]. 778 61

Atherosclerosis develops rapidly in patients with diabetes or renal insufficiency. Plasma lipoprotein profiles are frequently abnormal in these conditions and reflect an elevation in the level of the apoprotein B (ApoB)-containing components very low density lipoprotein (VLDL) and low density lipoprotein (LDL). High levels of circulating advanced glycation end products (AGEs) also occur in diabetes and end-stage renal disease (ESRD). These products arise from glucose-derived Amadori products and include AGE-modified peptides (AGE-peptides) which result from the catabolism of AGE-modified tissue proteins. AGE-peptides have been shown to crosslink protein amino groups and to accumulate in plasma as a consequence of renal insufficiency. To address potential mechanisms for the dyslipidemia of diabetes and ESRD, we investigated the possibility that circulating AGEs react directly with plasma lipoproteins to prevent their recognition by tissue LDL receptors. AGE-specific ELISA showed a significantly increased level of AGE-modified LDL in the plasma of diabetic or ESRD patients compared with normal controls. AGE-LDL formed readily in vitro when native LDL was incubated with either synthetic AGE-peptides or AGE-peptides isolated directly from patient plasma. LDL which had been modified by AGE-peptides in vitro to the same level of modification as that present in the plasma of diabetics with renal insufficiency exhibited markedly impaired clearance kinetics when injected into transgenic mice expressing the human LDL receptor. These data indicate that AGE modification significantly impairs LDL-receptor-mediated clearance mechanisms and may contribute to elevated LDL levels in patients with diabetes or renal insufficiency. This hypothesis was further supported by the observation that the administration of the advanced glycation inhibitor aminoguanidine to diabetic patients decreased circulating LDL levels by 28%.
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PMID:Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. 793 86

Lipoprotein lipase (LPL), a 55 kDa secretory glycoprotein produced in numerous tissues, is a hydrolytic enzyme, rate-limiting for the removal of lipoprotein TG from the circulation. It is activated by apoprotein CII present on TG-rich lipoproteins. It is involved in lipid transfer between lipoproteins, and plays an important role in the formation of HDL. The fate of LPL-derived lypolysis products differs between tissues: for instance, in adipose tissue, LPL-mediated delivery of free fatty acids is rate-limiting for TG storage, whereas in muscle it provides an alternate source of lipid fuel. LPL is regulated by hormones like insulin and nutrients; its activity depends on the metabolic state of the tissue. It has distinct roles in many normal tissues, such as adipocytes or muscles, as well as an important role in atherogenic dyslipidemia and in metabolic diseases including obesity and hypertriglyceridemia.
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PMID:[Lipoprotein lipase: a key enzyme of lipid metabolism]. 793 19

Diabetic patients have a 2 to 4 times higher risk of development of atherosclerosis than non-diabetic subjects. One of the risk factors of atherosclerosis is an impaired lipid and lipoprotein metabolism which is influenced by the type of diabetes, the degree of its metabolic compensation, character of treatment and other concurrently present metabolic abnormalities. In metabolically balanced type 1 diabetes the levels of commonly assessed lipoproteins do not differ from those in non-diabetic subjects, the HDL-cholesterol level can be even higher. The lipid profile of type 2 diabetics is not very homogeneous, however, usually elevated levels of VLDL-triglycerides and of apoprotein B and a reduced HDL-cholesterol level are found. At present there are no unequivocal views on the role of the lipoprotein (a) ratio in the increased risk of atherosclerosis in diabetics as investigations devoted to the lipoprotein (a) level and its relation to macrovascular complications in diabetes did not give unequivocal results. The scope of dyslipidemia in diabetics with nephropathy is in addition to the effect of the basic disease influenced also by the extent of renal damage. The lipid disorder, on the other hand, leads to deterioration of albuminuria and progression of the renal disease.
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PMID:[Changes in lipoprotein metabolism in patients with diabetes mellitus and the effect on lipid profile in diabetics]. 818 88

Fifteen patients on chronic maintenance hemodialysis without any additional known cause for dyslipidemia were arbitrarily divided into two groups based on fasting plasma triglyceride levels. The hypertriglyceridemic patients (plasma triglyceride levels above 170 mg/dl, N = 7) also had decreased high density lipoprotein (HDL) cholesterol levels and decreased post-heparin plasma lipoprotein lipase activity compared to the normotriglyceridemic patients (N = 8). All lipoprotein fractions collected by density gradient ultracentrifugation were triglyceride-enriched in the hypertriglyceridemic patients. Both groups of patients had elevated intermediate density lipoprotein levels, heterogeneity in the distribution of low density lipoproteins (LDL) and apoprotein-specific HDL subpopulations, and abnormalities in the size and composition of both LDL and HDL. The described alterations tended to be more marked in hypertriglyceridemic patients and are not detected by the usual laboratory evaluation of lipoproteins. These lipoprotein abnormalities have been shown to be atherogenic in patients without renal disease and are likely to contribute to the high prevalence of premature atherosclerosis in end-stage renal disease.
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PMID:Lipoprotein heterogeneity in end-stage renal disease. 844 Dec 37

Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.
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PMID:Atypical hyperlipidemia and nephropathy associated with apolipoprotein E homozygosity. 858 83


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