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)

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

Renal insufficiency is frequently associated with both quantitative and qualitative abnormalities in lipid and hemorheologic profiles. Although this may lead to increased risk of cardiovascular disease, a number of studies have also shown dyslipidemia to be a significant risk factor for the progression of renal insufficiency in human chronic renal disease. This double-blind, placebo-controlled trial aimed to assess the effect of fluvastatin, a synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on these parameters in dyslipidemic patients with or without chronic renal insufficiency. After a 6-week placebo run-in, 42 patients who had been previously stratified into 2 groups on the basis of creatinine clearance levels (0.5-1.0 mL/sec or > 1.0-1.5 mL/sec) were randomized to treatment with fluvastatin (40 mg daily) or matching placebo. Significant differences (on analysis of variance with repeated measures) were seen between fluvastatin and placebo treatment groups for changes in total cholesterol (-15% vs 1%, respectively; p < 0.001), low density lipoprotein cholesterol (LDL-C; -21% vs -5%; p < 0.001), very low density lipoprotein cholesterol (-14% vs 14%; p = 0.017), very low density lipoprotein triglycerides (-1% vs 29%; p = 0.014) and total triglycerides (-7% vs 24%; p < 0.001). These effects on cholesterol levels were reflected in a significant decrease in apolipoprotein B levels with fluvastatin therapy (p < 0.001). Apolipoprotein A-I levels increased (p = 0.054) despite no significant change in the levels of high density lipoprotein cholesterol. Response to therapy did not differ between the 2 renal function groups for any of the lipid, lipoprotein, and apolipoprotein variables. Hemorheologic parameters were not altered with fluvastatin therapy, regardless of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluvastatin for dyslipoproteinemia, with or without concomitant chronic renal insufficiency. 760 9

Atherosclerosis susceptibility associated with elevations in specific populations of apolipoprotein-B-containing particles may involve increased oxidation of lipoproteins and associated changes in their biological properties. Lipoprotein oxidation may be potentiated by the greater mass of oxidizable lipoprotein substrates, as well as by a greater intrinsic susceptibility of the specific forms of lipoproteins that arise in these disorders. The atherogenic consequences of increased lipoprotein oxidation may be further enhanced by a greater relative potency or toxicity of the oxidized products of these lipoprotein subpopulations. This review addresses these facets of lipoprotein oxidation in several forms of dyslipidemia, and in view of both differences between and commonalities among these disorders, proposes that lipoprotein oxidative behavior is determined by a complex array of physical, chemical, and metabolic factors.
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PMID:Lipoprotein oxidation in dyslipidemia: insights into general mechanisms affecting lipoprotein oxidative behavior. 767 Jul 48

Several lines of evidence suggest that a subset of women may be at increased risk of cardiovascular disease because of unfavorable alterations in insulin action and/or production, accompanying altered apolipoprotein metabolism and altered androgenicity and/or estrogenicity. A number of cardiovascular disease risk factors, including central obesity, insulin resistance (with associated hyperinsulinemia), dyslipidemia, and/or diabetes mellitus, tend to cluster in these women. Another common ovarian morphology in women with hyperandrogenism is polycystic ovaries, which cluster with hirsutism, anovulation, infertility, gonadotropin secretion abnormalities, android fat distribution, and many important cardiovascular disease risk factors. Studies indicate that androgen excess may be a signal of increased risk for coronary artery disease, even in younger women. If androgenicity and insulin resistance are early warning signs of increasing risk of morbidity and mortality, these patients are prime candidates for preventive medicine. It is important that primary care providers begin to recognize these androgen disorders as a clue to the existence of a complex, lifelong pattern potentially placing women at risk for premature morbidity and mortality and initiate preventive treatment before irreversible thresholds are crossed.
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PMID:Obesity, lipids, cardiovascular risk, and androgen excess. 782 38

Remnants of triglyceride-rich lipoproteins accumulate in plasma of subjects with type III hyperlipoproteinemia (HLP) due to defective clearance by hepatic receptors. Although most subjects with type III HLP are homozygous for apolipoprotein (apo) E2 (arg158-->cys, R158C), a variant that binds defectively to cell surface receptors, some individuals with type III HLP have rare mutations of apo E. We identified six subjects from three families with type III HLP who had either an apo E3/1 or E4/1 phenotype by isoelectric focusing. Using DNA restriction isotyping with HhaI, all six subjects were determined to have only one apo E allele encoding cys158 and the other encoding arg158. Subsequently, digestion of polymerase chain reaction-amplified portions of exon 4 of the apo E gene with endonucleases HaeIII, TaqI, and Sau3AI demonstrated a second DNA variant that encoded a single amino acid substitution (gly127-->asp, G127D) due to a guanosine-to-adenosine nucleotide change resulting in the apo E1 isoform (G127D, R158C), which had arisen from a parent apo E2 allele. This mutation was confirmed with direct DNA sequencing. Incubation of very low density lipoprotein (VLDL) isolated from hyperlipidemic apo E1 subjects with J774 macrophages resulted in a 7- to 12-fold increase in cellular cholesterol ester compared with VLDL from apo E2/2 subjects. Although heterozygosity for apo E1 alone did not impair the interaction of VLDL with cellular receptors in vitro, its presence in subjects with type III HLP suggests that apo E1, perhaps in combination with secondary factors, may be causative for the dyslipidemia.
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PMID:Identification, molecular characterization, and cellular studies of an apolipoprotein E mutant (E1) in three unrelated families with hyperlipidemia. 788 34

An understanding of lipoprotein metabolism in diabetes is essential because dyslipidemia contributes to the atherosclerotic process in diabetic individuals. Current work has centered on elucidating the compositional changes and apolipoprotein alterations of plasma lipoproteins that occur in diabetic individuals. Studies of the mechanisms responsible for the altered concentrations and composition are reviewed. There is an urgent need for more studies of therapeutic approaches to diabetic dyslipidemia.
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PMID:Lipoprotein metabolism in diabetes. 795 16

The lipid and lipoprotein profiles including apolipoprotein A1 and B100 are measured in 50 idiopathic nephrotic patients (males 26, females 24) with mean age of 32 + 13.6 yrs, serum creatinine 1.32 +/- 0.43 mg/dl compared with 50 age matched normal controls. The renal histology consist of IgM nephropathy 70 per cent, membranous 12 per cent, and IgA 2 per cent. The serum cholesterol, triglycerides, LDL- cholesterol, VLDL-cholesterol, apolipoprotein B (521.6 +/- 201.6, 291.4 +/- 156.2, 438.8 +/- 207.4, 58.3 +/- 31.2, 265.1 +/- 119.8) are statistically significantly higher than controls (p < 0.001). The HDL-cholesterol (30.2 +/- 16.1) is also significantly lower than controls (p < 0.001) but apolipoprotein A is not different from normal subjects. The most common hyperlipoprotein type is type IIb (66%), less common are type IIa (22%), IV (6%) and III (4%) respectively. There is no correlation between serum lipids, lipoproteins and urinary protein, serum albumin, and histological diagnosis. The ratio of cholesterol: HDL, LDL: HDL and Apo A1: B are all significantly higher than normal control (p < 0.001) and correlate with urinary protein levels. This study shows that the nephrotic patients who have persistent heavy proteinuria have dyslipidemia which is highly atherogenic and probably increases the incidence of coronary heart disease.
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PMID:Lipoprotein abnormalities in adult nephrotic syndrome. 796 58

Dyslipidemia is a common feature of renal failure. It is primarily caused by delayed catabolism of lipoprotein particles. This is due to decreased activity of the key enzymes of delipidation of lipoprotein particles (LPL, HTGL) and of HDL remodeling (LCAT). In epidemiological studies no correlation has been found in dialysis patients between total lipids and atherosclerotic endpoints and a modest relation, at best, between more sophisticated apolipoprotein indices and vascular disease. Such lack of correlations are presumably explained by malnutrition as a confounding factor. Fascinating new observations in animal studies document that in various models of renal damage, development of glomerulosclerosis is accelerated by hyperlipoproteinemia, either endogenous hyperlipoproteinemia or hyperlipoproteinemia induced by feeding of fat. Conversely, correction of hyperlipoproteinemia mitigates development of glomerulosclerosis. Currently there is no firm evidence that the same is true in humans.
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PMID:[Dyslipoproteinemia: its importance in nephrology]. 814 62

Hyperlipidemia is common in renal allograft recipients. To elucidate the role of cyclosporine in posttransplant hyperlipidemia, we measured lipids, lipoprotein lipids, and apolipoproteins of thirty-five renal allograft recipients and evaluated their relation to trough cyclosporine blood levels. All patients were on a triple immunosuppressive regimen with equal doses of prednisone and azathioprine, and had stable graft function. Cyclosporine blood levels were significantly correlated to total plasma cholesterol (P = 0.028), low-density lipoprotein cholesterol (P = 0.022), apolipoprotein B (P = 0.017), and the cholesterol/high-density lipoprotein cholesterol ratio (P < 0.002), but not to plasma triglycerides. Significant inverse correlations were found between cyclosporine blood levels and high-density lipoprotein cholesterol (P = 0.034), high-density lipoprotein3 cholesterol (P = 0.025), and apolipoprotein A-1 (P = 0.047), but not high-density lipoprotein2 cholesterol. The independent relation of cyclosporine blood levels to each of the measured lipid parameters was investigated by a stepwise regression model including age, body mass index, interval from transplantation, diabetes mellitus, plasma creatinine, and intake of diuretics and beta-blockers. After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. These data suggest that cyclosporine causes atherogenic dyslipidemia.
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PMID:Relation of cyclosporine blood levels to adverse effects on lipoproteins. 819 11

The effects of long-term monotherapy with felodipine, a calcium antagonist, on blood pressure, glucose tolerance, and serum lipid profiles were prospectively investigated in 51 hypertensive patients: 13 with normal glucose tolerance and 38 with glucose intolerance. The levels of plasma glucose, serum lipids, and glycosylated hemoglobin A1c were determined before and during long-term (7.5 +/- 0.5 months; range, 6 to 9 months) therapy with felodipine. A 75-g oral glucose tolerance test was performed before and during long-term felodipine therapy. Significant decreases in both systolic and diastolic blood pressures in both patient groups were maintained during the therapy. Neither fasting nor post-glucose load venous plasma glucose levels were altered in either group of patients, and no patients with normal glucose tolerance developed diabetes mellitus during the study. Serum lipid levels did not change significantly in either group of patients except for significant decreases in high-density lipoprotein cholesterol and apolipoprotein A-I in the group with normal glucose tolerance tests, but those changes remained within the normal range. Furthermore, neither serum lipid nor apolipoprotein levels were altered, even in patients with hypercholesterolemia (total cholesterol levels, > 5.69 mmol/L = 220 mg/dL). These results suggest that long-term therapy with felodipine may not alter glucose and lipid metabolism in hypertensive patients, and felodipine appears to be useful as an antihypertensive agent for hypertensive patients with either dyslipidemia or impaired glucose metabolism.
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PMID:Felodipine therapy may not alter glucose and lipid metabolism in hypertensives. Felodipine Multicenter Prospective Study Group in Japan. 828 62


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