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)

The appearance and accumulation of apolipoprotein B and unesterified cholesterol in the lesion-prone areas of the aorta in rabbits with diet-induced hyperlipidemia were investigated by histo-, and cytochemical techniques. Apolipoprotein B was detected by an indirect immunoperoxidase procedure both in the light and electron microscopy. Unesterified cholesterol was revealed using filipin and tomatine as specific probes. In the prelesional stages of atherogenesis, before the appearance of any structurally detectable lesions, as demonstrated by bright-field and fluorescence microscopy, apolipoprotein B and free cholesterol accumulated progressively in the extracellular matrix of the subendothelial space. At ultrastructural level, extracellular phospholipid liposomes, unesterified cholesterol and apolipoprotein B concomitantly appeared and accumulated focally in the same areas. Apolipoprotein B was preferentially located on the outer surface of the free cholesterol-containing phospholipid lamellae of the extracellular liposomes. In the lesional stages leading to fatty streak formation, the extracellular liposomes, apolipoprotein B and unesterified cholesterol had also topographically a superimposed localization pattern. Intracellular apolipoprotein B and unesterified cholesterol were also colocalized in some intimal lipid-laden cells. In the prelesional stages of hyperlipidemia the prevalent localization of apolipoprotein B around individual unesterified cholesterol-rich extracellular phospholipid liposomes, progressively accumulating in the subendothelial space, suggests their possible origin from serum-derived lipoproteins.
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PMID:Prelesional events in atherogenesis. Colocalization of apolipoprotein B, unesterified cholesterol and extracellular phospholipid liposomes in the aorta of hyperlipidemic rabbit. 331 87

The different types of serum lipoproteins, including apolipoprotein E phenotypes, were measured in 50 patients with xanthelasma. Half of them were found to be hyperlipemic. The normolipemic and hyperlipemic groups with xanthelasma were compared with two control groups (one a group of normolipemic patients and another a group of hyperlipemic patients without xanthelasma) selected as homogeneously as possible with regard to age, sex, degree of obesity, and hyperlipemic phenotype. The only significant differences found among the groups, regardless of the presence of hyperlipemia, were the increased levels of total and high-density lipoprotein phospholipids, and lower levels of apolipoprotein B, found in the group with xanthelasmas. The distribution of apolipoprotein E phenotypes was the same in both groups, with slight differences between the normolipemic and hyperlipemic groups. Patients with xanthelasmas showed slight deviations in the metabolism of lipoproteins that require further clarification.
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PMID:Apolipoprotein E phenotypes, lipoprotein composition, and xanthelasmas. 277 5

The purpose of this study was to compare the relative effects of omega-3 fatty acids (omega-3 FAs) in the triglyceride (TG) and methly ester (ME) forms in a crossover design in patients with type IV hyperlipidemia. Eight male patients were given 18 vegetable-oil capsules (control); 18 capsules of a TG rich in omega-3 FAs (omega-3 TG); and 11 capsules containing omega-3-FA MEs (omega-3 ME). One supplement was given during each of three 6-wk periods. Equivalent amounts of omega-3 FAs (6.8 g/d) were provided by each of the omega-3 treatments. Plasma cholesterol (C) levels were unchanged during the two omega-3 phases whereas plasma TG levels fell by 44% during both. Low-density-lipoprotein cholesterol (LDL-C) levels rose significantly with both omega-3-FA treatments, as did apolipoprotein B levels. When taken in either the TG or ME forms, omega-3 FAs are equally effective hypotriglyceridemic agents but they may raise LDL-C levels.
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PMID:Omega-3 fatty acids in hypertriglyceridemic patients: triglycerides vs methyl esters. 342 Dec 9

Pirozadil (pyridine 2,6-dimethanol-bis(3,4,5-trimethoxybenzoate), Pemix) was administered for 16 weeks at a dose of 1.5 or 2.0 g/d to 15 adults with Type IIa hyperlipidemia. All patients had achieved a stable weight and were given a diet before treatment. Plasma lipids, lipoproteins and apolipoproteins were measured at 4-week intervals. Pirozadil reduced the mean total cholesterol (TC) level from 291.0 mg/dl to 260.8 mg/dl in 16 weeks (p less than 0.05). The mean percentage decrease was 8.5% in week 16. Low density lipoprotein (LDL)-cholesterol and apolipoprotein B (apoB) decreased 9.7% and 8.5%, respectively, in week 16. A decrease of more than 10% in TC, representing a decrease of more than 30 mg/dl, was observed in 12 of the 15 patients. These 12 patients, who were regarded as responders, showed mean decreases in the levels of TC, LDL-cholesterol and apoB of 13.7%, 10.4% and 11.7%, respectively, but no significant change in the level of high density lipoprotein (HDL)-cholesterol or serum triglycerides. Eight of 11 patients in the lower dose group (1.5 g/d) and all 4 patients who had obtained the higher dose (2.0 g/d) were responders. Suspected side effects of pirozadil were edema, numbness of the extremities and palpitation. The results obtained suggest the beneficial effect of pirozadil on serum lipids in patients with Type IIa hyperlipoproteinemia.
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PMID:Effect of pirozadil on lipids, lipoproteins and apolipoproteins in Japanese with type IIa hyperlipoproteinemia. 343 4

An association between arterial blood pressure and blood viscosity has been suggested in healthy and in diabetic subjects, and that the hemorheological pattern may be influenced by blood lipid alterations. In diabetic patients a relationship between arterial hypertension and blood lipid changes may therefore be suggested. This study concerns 19 type II diabetics with hyperlipidemia (triglycerides = 3.2 +/- 1 mmol/l; total cholesterol = 6.1 +/- 1.2 mmol/l; HDL-cholesterol = 0.92 +/- 0.27 mmol/l; VLDL = 29 +/- 5%) (group A), and 19 normolipidemic type II diabetics (triglycerides = 1.15 +/- 0.5 mmol/l; total cholesterol = 5.1 +/- 1 mmol/l; HDL-cholesterol = 1.25 +/- 0.38 mmol/l; VLDL = 20 +/- 5%) (group B). No differences concerning age, body weight, duration of diabetes and glycemic control were found in hyperlipidemic compared to normolipidemic diabetics. On the contrary, higher systolic and diastolic blood pressure levels were demonstrated in group A (167 +/- 14 mmHg and 101 +/- 5.2 mmHg, respectively) than in group B (144 +/- 15 mmHg, p less than 0.001 and 87 +/- 6.9 mmHg, p less than 0.001, respectively). An increase of plasma apolipoprotein B level (163 +/- 27 mg/dl vs 102 +/- 21 mg/dl, p less than 0.001), of plasma viscosity (1.81 +/- 0.08 mPas vs 1.51 +/- 0.07 mPas, p less than 0.001) and of blood viscosity (5.37 +/- 0.33 mPas vs 5.07 +/- 0.04 mPas, p less than 0.01, at shear-rate of 90 s-1; 18.4 +/- 1 mPas vs 14.1 +/- 0.9 mPas, p less than 0.001 at shear-rate of 2.25 s-1) was found in group A, compared to group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased plasma apolipoprotein B levels and blood hyperviscosity in non-insulin-dependent diabetic patients: role in the occurrence of arterial hypertension. 343 3

A child showed a type IIb lipoprotein pattern and triglyceride-enriched cutaneous xanthomas before 1 year of age. The proband and 9 of 18 relatives had elevated plasma levels of low density lipoprotein (LDL) B protein; of these nine relatives, four had elevated LDL of increased density while five had elevated LDL of normal density. Compared with normal LDL, LDL of increased density had less cholesteryl ester and free cholesterol, more apolipoprotein B and triglyceride, and a lower molecular weight and flotation rate (Sf degrees). Patients with LDL of increased density had higher mean plasma levels of triglycerides, very low density lipoproteins, and intermediate density lipoproteins, but lower levels of high density lipoproteins than those with elevated LDL of normal density. Multiple lipoprotein patterns in the father's family suggested the presence of familial combined hyperlipidemia (FCH). The mother of the proband and two of her relatives had type IIa lipoprotein patterns and tendon xanthomas, compatible with familial hypercholesterolemia (FH). High affinity binding, internalization, and degradation of 125I LDL in cultured fibroblasts from the proband and his mother were reduced two- to threefold compared with normal cells, while LDL receptor activity in the proband's father was normal. This unusual proband has apparently inherited both FCH and FH.
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PMID:Hyperapobetalipoproteinemia in a kindred with familial combined hyperlipidemia and familial hypercholesterolemia. 359 67

Cholesteryl ester storage disease (CESD) is characterized by the deficient activity of lysosomal cholesteryl ester (CE) hydrolase, accumulation of LDL-derived CE in lysosomes, and hyperlipidemia. We studied the kinetics of VLDL and LDL apolipoprotein B (apoB), using 125I-VLDL and 131I-LDL, in a 9-yr-old female with CESD and elevated total cholesterol (TC) (271.0 +/- 4.4 mg/dl), triglyceride (TG) (150.0 +/- 7.8 mg/dl), and LDL cholesterol (184.7 +/- 3.4 mg/dl). These studies demonstrated a markedly elevated production rate (PR) of apoB, primarily in LDL, with normal fractional catabolism of apoB in VLDL and LDL. Urine mevalonate levels were elevated, indicative of increased synthesis of endogenous cholesterol. Treatment with lovastatin, a competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase, resulted in significant reductions in TC (196.8 +/- 7.9 mg/dl), TG (100.8 +/- 20.6 mg/dl), and LDL cholesterol (102.0 +/- 10.9 mg/dl). Therapy reduced VLDL apoB PR (5.2 vs. 12.2 mg/kg per d pretreatment) and LDL apoB PR (12.7 vs. 24.2 mg/kg per d pretreatment). Urine mevalonate levels also decreased during therapy. These results indicate that, in CESD, the inability to release free cholesterol from lysosomal CE resulted in elevated synthesis of endogenous cholesterol and increased production of apoB-containing lipoproteins. Lovastatin reduced both the rate of cholesterol synthesis and the secretion of apoB-containing lipoproteins.
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PMID:Suppression of apolipoprotein B production during treatment of cholesteryl ester storage disease with lovastatin. Implications for regulation of apolipoprotein B synthesis. 368 May 22

Anthropometric measurements, sixteen specific plasma proteins, triglycerides, cholesterol, urea and creatinine were measured at 4-monthly intervals for 1 year in 15 patients on CAPD. Delayed hypersensitivity skin tests were performed on 11 patients at the start and after 4 and 12 months. Body weight increased due mainly to a mean increase in 'calculated' body fat of 2.0 kg with increases in cholesterol, triglycerides and apolipoprotein B. Gain in fat correlated with the daily supply of dextrose in the dialysis fluid. Albumin, transferrin, prealbumin and retinol-binding protein decreased in 8 patients who intermittently ate less than 1.3 g protein/kg/day. A high concentration of dextrose in the dialysis fluid probably caused loss of appetite. Peritonitis resulted in increases in acute phase proteins although other plasma proteins decreased. Skin test responses indicated improvement in cell-mediated immunity during continuous ambulatory peritoneal dialysis (CAPD). The incidence of peritonitis and length of stay in hospital were greater in the patients who were hypoalbuminaemic probably due to impairment of the humoral mechanism. Dextrose in dialysis fluid may contribute to hyperlipidaemia and malnutrition with impairment of immunocompetence.
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PMID:Nutrition and delayed hypersensitivity during continuous ambulatory peritoneal dialysis in relation to peritonitis. 372 25

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
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PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

Low density lipoprotein (LDL) is probably the most atherogenic of all the lipoproteins. Several abnormalities in LDL metabolism seem to be associated with coronary heart disease (CHD) one of them being an elevation of plasma LDL concentration. Recent findings suggest that disorders in the metabolism of LDL could be associated with accelerated atherosclerosis even without elevated LDL levels such as increased flux of LDL and changes in the LDL composition. Elevation of plasma LDL levels can be caused by two factors, first, a decrease in the clearance of LDL and second, an overproduction of this lipoprotein. Catabolism of LDL is largely determined by the LDL receptors as clearly shown in patients with familial hypercholesterolemia (FH). In this inherited disease the patients do not have normal LDL receptors and their LDL levels are remarkably elevated. LDL production is also increased in these subjects. In the rest of the population LDL levels are regulated by both the LDL clearance and production rate. The latter also seems to be related to the LDL receptor activity. The conversion of the LDL precursor, very low density lipoprotein (VLDL) to LDL is the most important factor regulating LDL synthesis. When the LDL receptor activity is low a large fraction of VLDL apolipoprotein B (apoB), the major structural protein in VLDL, is converted to LDL, and LDL production is high. On the other hand, only a small part of VLDL apoB is converted to LDL resulting in low LDL synthesis rate in conditions with high LDL receptor activity. The relationships between production and clearance of LDL are, however, more complex. There are individuals who produce a large number of VLDL and LDL particles but maintain LDL concentrations at a normal level by clearing their LDL very effectively. These subjects obviously have another abnormality in lipoprotein metabolism namely an overproduction of apoB. This disorder has been observed in several conditions like obesity, adult-onset diabetes mellitus, several patients with familial combined hyperlipidemia and some normolipidemic subjects with premature coronary heart disease. In all these conditions increased transport of LDL can be associated with coronary artery disease even in the absence of hypercholesterolemia. This raises the possibility that increased flux of LDL could itself be atherogenic possibly by overloading reverse cholesterol transport. Finally, there is some evidence that LDL particle composition may be important in the process of atherogenesis. High LDL apoB but normal LDL cholesterol levels, hyperapobetalipoproteinemia, has been associated with premature coronary heart disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Abnormalities in metabolism of low density lipoproteins associated with coronary heart disease. 390 93


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