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)

1. Hypertriglyceridemia and hyper beta-lipoproteinemia are closely related to the pathophysiologic status of the cerebrovascular patients. 2. The electrophoretic analysis of serum lipoprotein is the usefull method for the study on hyperlipidemia in the cerebrovascular disease. 3. The electrophoretic analysis of the serum lipoprotein gives close relation to the clinical features in the patients with normal serum lipid levels as well as in those with the hyperlipidemia. 4. Hyperlipidemia relates closely to the renal impairment, which is supposed to originate from the sclerotic changes of renal artery.
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PMID:Hyperlipidemia in cerebrovascular diseases. 16 33

A 48 year old male patient presented with xanthomatosis, hyperbeta lipoproteinemia and hyper-IgA globulinemia; these two serum components occurred as a "complex." The patient has subsequently been studied for 22 years (1952 to 1974). His serum cholesterol and triglyceride levels have been consistently and excessively high despite efforts to regulate them by means of diet or diet and drugs. Serum immunoglobulin A (IgA) concentration ranged from 1,400 to 3,400 mg/dl compared with a normal value of 156 plus or minus 92 mg/dl. The metabolism of lipoproteins, judged by vitamin A turnover studies was slow. Peripheral atherosclerosis became evident 15 years after beginning the study whereas cinecoronary arteriography concurrently demonstrated only minimum changes. Xanthomas exhibited marked regression only during the last 6 years, after 16 years of diet and the addition of clofibrate for 7 years. Beta lipoprotein and IgA globulin determined by immunofluorescent and immunoelectrophoretic technics were demonstrated in the atherosclerotic material obtained from the patient's arterial wall. They were also found in the plasma cells of the bone marrow. The IgA globulin-beta lipoprotein complex in the serum was broken with difficulty. The patient's isolated IgA globulin, free of lipoprotein, formed a firm complex when mixed with beta lipoprotein prepared from normal human serum. Initially, IgA globulin studies showed presence of both kappa and lambda light chains in normal proportion. But after 18 years, the IgA globulin has become monoclonal, type lambda. The plasma cells of the bone marrow have become progressively more atypical and immature. No clinical indications of multiple myeloma have been found. It is concluded that association of lipoproteins with IgA globulin in the serum of this patient with hyperlipidemia, hyper-IgA globulinemia did not prevent the development of atherosclerotic lesions and the deposition of lipids and lipoproteins in the plaques. It is possible that the lipoprotein-immunoglobulin association may have retarded the process, since it became manifest only after many years of known hyperlipidemia.
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PMID:Autoimmune hyperlipidemia in a patient. Atherosclerotic course and chaning immunoglobulin pattern during 21 years of study. 16 71

Experimental models for hyper-beta-lipoproteinemia were established in rats and the effects of certain hypolipidemic drugs were studied with these models. In the hyperlipemia induced in rats by feeding a high cholesterol diet, Y-9738 [ethyl 2(4-chlorophenyl)-5-ethoxy-4-oxazoleacetate] produced a dose-dependent reduction of serum cholesterol: such hypolipidemic activity was estimated to be about 7 times as great as that of clofibrate. On the other hand, clofibrate induced hepatomegaly at 100 mg/kg, whereas Y-9738 did not at this dosage, which is about 10 times the effective dose. Hyperlipemia induced by high cholesterol and thiouracil was characterized by increased beta-lipoprotein (heparin-calcium and disc electrophoresis). In this model, Y-9738 showed a dose-dependent lowering effect on beta-lipoprotein cholesterol with a marked decrease in the beta/alpha lipoprotein ratio. A tendency was noted for alpha-lipoprotein to be increased. In contrast, clofibrate exerted no effect on this hyper-beta-lipoproteinemia. These results suggest that the above models may be of value in exploring hyper-beta-lipoproteinemia and that Y-9738 may be more useful than clofibrate in the therapy of hyperlipemia.
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PMID:Experimental hyper-beta-lipoproteinemia and its amelioration by a novel hypolipidemic agent. 20 4

Uremic patients on prolonged maintenance hemodialysis (hemodialysis patients) are at high risk for atherosclerotic cardiovascular complications. To investigate the serum lipoprotein (Lp) abnormalities in hemodialysis patients, high density Lp (HDL) concentration was determined using ultracentrifugal analysis and quantitative immunoelectrophoresis in 23 hemodialysis patients, 8 non-uremic hyperlipidemic subjects, and 12 normal subjects. Immunoreactive HDL as well as HDL-cholesterol (HDL-Ch) in hemodialysis patients was lower significantly than the level in patients with non-uremic hyperlipidemia or normolipidemic healthy persons. Taking the results of previous reports into counts, decrease in HDL and HDL-Ch seems to contribute to the development of dyslipoproteinemia (broad-midband lipoproteinemia; an accumulation of the intermediate Lp or the remnant Lps) in hemodialysis patients. The results of the present study suggest that protective function proposed by the previous workers of HDL against atherosclerosis may be operated by facilitating the elimination of the accumulated midband Lps.
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PMID:Serum high density lipoprotein in hemodialysis patients. 21 23

The influence of experimentally induced hyperlipidemia and aging on the development of pulmonary foam cells (PFCs) was examined in Fischer 344 rats. The male and female rats were administered orally with cholesterol at a dosage level of 1000 mg/kg/day for 30 days from 6 to 10 weeks or from 33 to 37 weeks of age. The control rats received the vehicle only in the same manner. Plasma levels of total cholesterol, phospholipid, triglyceride (TG), beta-lipoprotein (beta-LP) and calcium in both control and cholesterol-administered groups were higher at 37 weeks than at 10 weeks of age. Plasma beta-LP and TG levels in the treated groups were significantly higher or tended to be higher than those of the controls at 10 and 37 weeks of age. Males of the treated group showed the highest level of beta-LP at 37 weeks of age, positively correlated with the highest incidence of PFCs. PFCs developed singly or in a small cluster in peribronchial and subpleural regions. PFCs had an abundant cytoplasm filled with many fine vacuoles containing neutral lipid and cholesterol. PFCs stained with PAS and reacted immunohistochemically with both anti-rat monocytes/macrophages monoclonal antibody and anti-lysozyme antibody. Moderately swollen macrophages with a foamy appearance were detected in perivascular connective tissues of the lungs and they were considered to represent an initial stage of the development of PFCs. These observations suggest that hyperlipidemic conditions, particularly hyper beta-lipoproteinemia, resulting from cholesterol administration or aging may be involved in the development of PFCs in rats.
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PMID:Influence of cholesterol administration and aging on the development of pulmonary foam cells in F344 rats. 260 22

.ur current model for cholesterol transport is summarized in Figure 10. In this figure we have put together the various steps in cholesterol transport that were described previously in this review. Under normal conditions, cholesterol metabolism and transport are well regulated. If the transport system is overloaded for a long time, however, hypercholesterolemia caused mainly by increased plasma LDL may develop in several species, including humans. Under such circumstances reverse transport of cholesterol may also fail, giving rise to deposits of cholesterol. Tissue macrophages may be responsible for this lipid accumulation, because receptor-mediated (adsorptive) endocytosis of lipoprotein-associated cholesterol in these cells is not under negative-feedback control. The deposits are mainly found in tissues poorly supplied with blood and lymph: the skin, tendons, the cornea, and arteries. Overload of cholesterol transport may be the result of too much fat and cholesterol in the diet, giving rise to cholesterol-rich lipoproteins from the gut and to increased production of liver (formula; see text) VLDL, which in humans ends up as LDL. In many individuals, however, no hypercholesterolemia is seen, even after eating large amounts of a "western" diet for decades; others may develop increased LDL on a relatively "prudent" diet. Obviously many of the factors and mechanisms in cholesterol transport are influenced by genetic factors. Although studies of several inborn errors of lipid metabolism have given information about some mechanisms, the quantitatively more important differences in genetic patterns, which determine whether or not a western diet will result in hyperlipidemia, are not well known. Perhaps studies of different forms of apoB and apoE and of HDL subgroups and hyper-alpha-lipoproteinemia will explain why certain individuals develop hypercholesterolemia and premature atherosclerosis. All the recent information related to cholesterol metabolism and transport gives rise to new questions. There are many problems of interest for future research: What are the metabolic differences between the apoB produced in the liver and that produced in the gut? To what extent is the protein moiety of LDL modified in the plasma of blood and lymph and in interstitial tissue? Are such modifications important to whether LDL uptake goes through the classic LDL pathway or through the macrophage (i.e., scavenger?) pathway? Are some changes in apoB important for liver recognition of LDL?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Transport of cholesterol. 636 11

On a diet with high levels of cholesterol and sucrose, a beta-lipoproteinemia developed in rhesus monkeys that is similar to type II human hyperlipidemia. Lesion regression appeared in response to drastic lowering of serum cholesterol (SC) levels. This experiment analyzed angiochemical responses on the addition of a bile-acid sequestrant to continued atherogenic feeding, which resulted in ranges of moderate cholesterolemia that mimick those that occur in man. After two years of atherogenic diet, fatty fibrous plaques were demonstrated in ten monkeys; then cholestyramine resin, 1.5 g/100 g of the atherosclerotic diet, was added to the food of eight monkeys, whereas two served as controls during a 12-month regression period. Six adult control monkeys that did not receive the atherosclerotic diet were also killed. Seven experimental animals overall showed plaque regression when SC level fell from 400 +/- 130 to 237 +/- 74 mg/dL; one animal showed angiographic combinations of progression and regression. Angiochemical evaluation demonstrated discordant data with instances of decreased plaque cholesterol content and increased levels of collagen. On the average, plaque regression and final composition were related to absolute levels of SC reduction induced by cholestyramine. Regression required that the threshold levels of cholesterol be below 200 mg/dL. Plaques regressed mainly by lipid absorption; in this experiment and, in particular, arterial segments, collagen content sometimes increased.
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PMID:Regression of atherosclerotic plaques in rhesus monkeys. Angiographic, morphologic, and angiochemical changes. 743 21

Double pre-beta lipoproteinemia (DPBL) is a plasma lipoprotein phenotype characterized by the presence of two agarose gel electrophoretic populations of very low density lipoproteins (VLDLs, d < 1.006 g/mL), i.e., normal pre-beta-migrating VLDL and slow pre-beta VLDL. Slow pre-beta VLDL represents remnant lipoproteins derived from the hydrolysis of triglyceride (TG)-rich lipoproteins (TRLs), and thus DPBL is a characteristic of plasma remnant lipoprotein accumulation. To determine the prevalence of DPBL in our lipid clinic population, patients (n = 2501) were selected who (1) had an unambiguous VLDL electrophoretic phenotype and could be classified as having either DPBL (DPBL+), beta-migrating VLDL (beta-VLDL +), or an absence of both (DPBL/beta-VLDL-/-) and (2) had hypercholesterolemia (HC: plasma cholesterol > or = 6.2 mmol/L, n = 1017), hypertriglyceridemia (HTG: plasma TG > or = 2.3 mmol/L but < 15 mmol/L, n = 554) or combined hyperlipidemia (HC + HTG, n = 930). Patients with TG < 2.3 mmol/L and cholesterol < 5.2 mmol/L acted as control subjects (n = 343). Using a commercially available agarose gel electrophoresis system, we identified 220 hyperlipidemic patients (8.8%) with DPBL (versus < 1% of control). The prevalence of DPBL was higher in (1) male than in female patients (10.7% versus 6.7%), (2) postmenopausal than in premenopausal females (7.3% versus 4.1%), and (3) patients with HC + HTG than in those with HTG or HC alone (15.8% versus 8.3% versus 2.7%, respectively). Patients with an epsilon 2 allele had a higher prevalence of DPBL; i.e., 26.9% of apoE 3/2 and 26.2% of apoE 4/2 patients had DPBL compared with 6.5%, 6.8%, and 7.4% of apoE 3/3, 4/3, and 4/4 patients, respectively. DPBL patients consistently had increased levels of VLDL-C and (LDL + HDL)-TG and decreased levels of LDL-C, and their plasma lipid profiles were intermediate between those of beta-VLDL+ and DPBL/beta-VLDL -/- patients. These results demonstrate that male sex, postmenopausal status in women, and the presence of an apoE 3/2 or apoE 4/2 phenotype are associated with an increased incidence of DPBL in hyperlipidemic patients.
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PMID:Prevalence of double pre-beta lipoproteinemia in hyperlipidemic patients is influenced by gender, menopausal status, and ApoE phenotype. 940 36

We established a strategy to directly measure cholesterol and triglyceride levels of each lipoprotein fraction using a combination of agarose gel electrophoresis and differential staining. The cholesterol and triglyceride levels determined by electrophoresis correlated significantly with those of ultracentrifugation. The correlation coefficients between these methods were, for cholesterol levels 0.975(very low density lipoproteins, VLDL), 0.986(low density lipoproteins, LDL) and 0.965(high density lipoproteins, HDL) and for triglyceride levels 0.994(VLDL), 0.963(LDL) and 0.959(HDL) respectively. Both intra-and inter-assays showed low values of coefficients of variation (CV) (less than 3.57%). We observed a strong linearity between staining and triglyceride concentration. An increased VLDL-cholesterol was observed in type III subjects, a result which enabled distinction between type III and type IIb or type V lipoproteinemia. The method revealed lipoprotein patterns in some samples otherwise unexpected from their corresponding serum lipid parameters. Analyses of these electrophoretic patterns thus provide an effective technique to classify types of hyperlipidemia defined by the WHO. Furthermore, quantitative measurement of chylomicrons, usually difficult, proved to be achievable, providing an additional analysis of postprandial hyperlipidemia and the exact measurement of LDL-cholesterol after diet. Consequently, we recommend this simple and easy method for clinical evaluation of abnormalities in lipoprotein profiles.
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PMID:Lipoprotein analysis using agarose gel electrophoresis and differential staining of lipids. 1168 14

The most common lipoprotein abnormality in type 2 diabetics is hypertriglyceridemia, which is known to be an independent risk factor for coronary artery disease (CAD) in diabetics. It is known that remnant lipoproteins, small, dense LDL, and isolated hypo-alphalipoproteinemia exist in diabetics even if they are apparently normolipidemic. Our previous observation revealed that type 2 diabetics had smaller LDL even if they were without hyperlipidemia. We also found that diabetics with microalbuminuria had smaller LDL than those with normoalbuminuria, indicating early nephrotoxicity of small, dense LDL. More than half of the Japanese type 2 diabetics associated with acute myocardial infarction (AMI) showed isolated hypo-alpha lipoproteinemia, indicating the clinical importance of suppressed HDL fraction without prominent hyperlipidemia in the diabetics. Finally, strict diet control and treatment of diabetics with dyslipidemias by acarbose, troglitazone, fibrates and/or statins were all successful in increasing LDL size.
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PMID:Atherogenic lipoproteins and diabetes mellitus. 1187 63


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