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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipidaemia, in particular raised concentrations of serum triglycerides, together with raised plasma non-esterified fatty acid concentrations, is common in patients with Type 2 (non-insulin-dependent) diabetes mellitus and may be associated with insulin insensitivity. Thirty non-obese Type 2 diabetic patients (15 controlled with diet alone and 15 with diet plus oral sulphonylurea therapy) were therefore recruited to take part in a double-blind, randomized, crossover comparison of acipimox (250 mg three times daily for 3 months) and placebo. Serum lipids, blood glucose control, insulin sensitivity, and glucose tolerance were measured before and after each treatment period. There was a significant decrease in serum triglycerides (2.05 +/- 1.08 vs 2.91 +/- 1.75: p < 0.005), cholesterol (5.66 +/- 1.02 vs 6.26 +/- 1.17: p = 0.0005), and apoprotein B (1.32 +/- 0.23 vs 1.44 +/- 0.25: p < 0.05) while HDL cholesterol and apoprotein A-1 concentrations were unchanged. There was no change in blood glucose control measured by fasting glucose, insulin, and HBA, concentrations, but there was a significant improvement in insulin action assessed by glucose-insulin infusion. Although plasma non-esterified fatty acid concentrations were lower during the oral glucose tolerance test after acipimox, there was no difference in either the peak or 2-h plasma glucose concentrations and the total area under the glucose curve did not change. Acipimox was well tolerated and no patients withdrew from the study for drug-related symptoms. Thus, acipimox effectively lowers serum cholesterol and triglycerides in patients with Type 2 diabetes without adversely altering blood glucose control, and appears to improve insulin sensitivity.
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PMID:A double blind study of the effect of acipimox on serum lipids, blood glucose control and insulin action in non-obese patients with type 2 diabetes mellitus. 147 35

Twenty-five patients with a renal transplant for 15 months to 19.4 years, hyperlipidaemia and stable graft function underwent three months of dietary management. Plasma lipid and apolipoprotein concentrations and lipoprotein electrophoresis were measured after a 12 hour fast at enrollment and after three months of diet. The aims of diet were to reduce energy intake in the overweight, restrict fat to 25-30% of total intake, reduce saturated fat content to less than 10% of total energy and cholesterol to less than 300 mg/d. After three months of diet there was a significant fall in mean cholesterol/HDL cholesterol risk ratio and a rise in mean HDL cholesterol concentration. Six patients reverted to a normal lipoprotein electrophoretic pattern with a significant reduction in mean total cholesterol, LDL cholesterol, cholesterol/HDL cholesterol ratio, apoprotein B and apoB/apo A-1 ratio. Most of the other patients who made dietary modifications showed some improvement in their lipid parameters. Dietary modification should be the initial approach to the management of posttransplant hyperlipidaemia.
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PMID:Effect of diet on posttransplant hyperlipidaemia. 154 40

The side effect profiles and lipid lowering efficacy of nicotinic acid (1 g three times daily) and its analogue acipimox (250 mg three times daily) in type 2b hyperlipidaemia were compared in a double-blind placebo controlled study. In the nicotinic acid group (n = 7) at 12 weeks there were significant reductions (P less than 0.05) with respect to placebo (n = 9) in total cholesterol (median and range) 6.6 mmol l-1 (4.8-8.4) vs 8.8 mmol l-1 (7.5-9.5), triglyceride 1.4 mmol l-1 (0.5-4.6) vs 2.8 mmol l-1 (1.5-9.5) and apoprotein B 88.6 mg dl-1 (62.1-114) vs 121.9 mg dl-1 (88.0-170.7). In contrast there was no significant alteration in lipids in the acipimox group (n = 12). Nicotinic acid was associated with a high incidence of side effects, principally cutaneous flushing, while acipimox was well tolerated by all patients.
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PMID:A comparison of acipimox and nicotinic acid in type 2b hyperlipidaemia. 157 71

A simple and high resolution procedure of apoprotein E (apo E) phenotyping by isoelectric focusing with immobilized pH gradients and silver staining is described. This method needs delipidated very low density lipoproteins (isolated from 1 mL of serum) but obviates immunoblotting as well as neuraminidase treatment in routine applications because the sialylated forms are clearly separated. Immunoblotting (with polyclonal and monoclonal anti-apo E antiserum), cysteamine and neuraminidase treatment, and pI markers allowed the localization of three main alleles, xi 2, xi 3, xi 4 and the detection of variants or rare alleles (6/450 determinations). The serum amyloid A (SAA) apolipoproteins (SAA1,SAA2) could be characterized unequivocally (especially with E3 and E4). Silver staining proved more sensitive than Coomassie Brilliant Blue and needs only 5 micrograms of protein in the sample. The results of 403 normo-or hyperlipidemic patients are shown. In the group of 191 normolipidemic patients (cholesterol less than 6.40 mmol/L triglycerides less than 2 mmol/L), the relative frequency of the xi 3 allele (0.83) is higher than in other reports on Caucasians (about 0.77) whereas the xi 4 allele is lower. As previously described, we find a high frequency of the 4/3 phenotype in hypercholesterolemia and 3/2 in hypertriglyceridemia. The high frequency of the E2/E2 phenotype, usually associated with hyperlipidemia, and variants in complex hypertriglyceridemia makes the apo E phenotyping necessary in many cases of dyslipidemias.
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PMID:Apolipoprotein E phenotyping by isoelectric focusing in immobilized pH gradients and silver staining. 162 6

The ability of sodium metavanadate to reverse the effects of streptozotocin-induced diabetes on hepatic cytochrome P-450 isozymes was examined in male rats. Streptozotocin caused P-450h levels to fall 95%, and P-450j and P-450b levels to rise 8- and 40-fold, respectively, after 1 week. When diabetic rats were administered metavanadate in the drinking water for 7 days, P-450h apoprotein and mRNA levels remained no different from those of untreated diabetic rats, whereas levels of P-450b and P-450j decreased toward those of control rats. Metavanadate also lowered serum triglyceride and 3-hydroxybutyrate levels without lowering serum glucose in the diabetic rats. Furthermore, P-450h mRNA levels correlated well with levels of P-450h apoprotein for all treatment groups, indicating that P-450h suppression in diabetic rats is under pretranslational control and is independent of the increased expressions of P-450j and P-450b, and of the hyperlipidemia and ketosis that occurs in diabetes. Vanadate is capable of separating the effects of diabetes on expression of individual P-450 isozymes.
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PMID:Effects of vanadate on hepatic cytochrome P-450 expression in streptozotocin-diabetic rats. 169 38

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
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PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

The postprandial response to three test meals provided during a single day was investigated in subjects with either the apo E3/3 phenotype (n = 8), or the apo E4/3 phenotype (n = 4), who had LDL-C greater than 160 mg/dl. Vitamin A (60,000 U/m2) was ingested with the first meal and retinyl palmitate determined four hours later. Triglyceride and total cholesterol concentration were determined on whole plasma and total cholesterol and free cholesterol determined following single spin ultracentrifugation (d less than 1.006 g/ml) and dextran precipitation of the d greater than 1.006 fraction to separate apoprotein-B containing lipoproteins. Fasting values revealed significantly lower HDL-cholesterol ester (p less than 0.03) and HDL3-cholesterol ester (p less than 0.03) and significantly greater HDL-free cholesterol (p less than 0.03) and HDL3-free cholesterol (p less than 0.02) in subjects with the E4/3 phenotype. Four hour postprandial HDL and HDL3 cholesterol ester increased significantly more (p less than 0.05) in E4/3 patients and HDL and HDL3 free cholesterol decreased significantly more (p less than 0.05) in E4/3 subjects. Eight-hour postprandial change values maintained the significant HDL3-cholesterol ester and free cholesterol difference, and, revealed a significantly greater triglyceride rich lipoprotein cholesterol ester reduction (p less than 0.01) in the E4/3 group. Individuals with the apolipoprotein E4/3 phenotype reveal significant differences in postprandial lipemia compared to individuals with the E3/3 phenotype, and, postprandial lipemia following multiple meals reveals differences not apparent from responses to a single meal.
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PMID:The effect of apolipoprotein E isoform difference on postprandial lipoprotein in patients matched for triglycerides, LDL-cholesterol, and HDL-cholesterol. 175 Aug 4

In recent years, LDL-apheresis has emerged to be an efficient treatment of hyperlipidemia in patients who do not respond sufficiently to diet and lipid lowering drugs. A survey of LDL lowering extracorporeal procedures is presented. Among them, to date 5 procedures have been used clinically on a routine basis: unselective plasma exchange, semi-selective double filtration (including its modifications like thermofiltration and predilution/backflush) and three highly selective LDL-apheresis systems: LDL-adsorption on dextran sulfate coated cellulose beads or anti-apoprotein B-linked sepharose and heparin induced extracorporeal LDL and fibrinogen precipitation (the so-called HELP system). Advantages, limitations and special indications of these commercially available systems are discussed. If atherosclerosis can really be made regress by drastic reduction of elevated serum cholesterol levels as indicated by recent publications, lipid apheresis will no doubt play a major role in attaining this goal.
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PMID:Overview: techniques and indications of LDL-apheresis. 175 62

The present study demonstrates very high levels of plasma lipids and high density lipoprotein (HDL) apolipoproteins (apoA-I and apoE) in female Nagase analbuminemic rats (NAR) fed a semi-synthetic diet in order to further increase the hyperlipidemia present in this strain. Plasma apoB-containing lipoproteins (very low, intermediate, and low density lipoproteins) were also elevated in NAR. Plasma cholesterol was mainly present in lipoprotein particles with a density between 1.02 and 1.12 g/ml. Separation of lipoprotein classes by gel filtration showed that the major cholesterol-carrying lipoprotein fractions in NAR plasma are apoE-rich HDL and apoA-I-rich HDL. The high HDL levels in NAR are explained, at least partly, by the two- to threefold elevated activity of plasma lecithin:cholesterol acyltransferase (LCAT). The lysophosphatidylcholine generated in the LCAT reaction, as well as plasma free fatty acids, are bound to lipoproteins in NAR plasma. A study was carried out to determine whether the elevated LDL and aopoE-rich HDL levels could be corrected by administration of the HMG-CoA reductase inhibitor pravastatin (at a dose of 1 mg/kg per day). Pravastatin treatment results in a 43% decrease in plasma triglycerides in NAR, but not in Sprague-Dawley (SDR) rats, and had no significant effect on plasma total cholesterol, phospholipids apolipoproteins A-I, A-IV, B, or E, as well as on plasma LCAT activity levels in NAR or SDR.
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PMID:Hyperlipoproteinemia in Nagase analbuminemic rats: effects of pravastatin on plasma (apo)lipoproteins and lecithin:cholesterol acyltransferase activity. 177 Feb 92

Hyperlipidemia associated with nephrotic syndrome was treated with probucol and the changes in plasma lipoprotein lipid concentration and urinary protein excretion were examined in puromycin aminonucleoside-induced nephrotic rats. Rats made nephrotic exhibited severe hyperlipidemia with increases in all major lipoprotein fractions. Probucol treatment of nephrotic rats significantly lowered plasma triglyceride (TG), cholesterol (Ch) phospholipid (PL) and apoprotein B associated with very-low-density and low-density lipoprotein and Ch and PL in high-density lipoprotein (HDL). Malondialdehyde (MDA) associated with the lipoproteins was significantly elevated in nephrotic rats and probucol treatment also lowered MDA concentration in all major lipoproteins. In control rats probucol moderately, but significantly, reduced plasma TG and HDL-Ch concentrations. Proteinuria associated with nephrosis was decreased significantly by treatment with probucol. Probucol treatment did not affect blood urea nitrogen and plasma creatinine levels. A significant positive correlation existed between the amount of protein excreted in urine and the plasma lipid concentrations in all nephrotic rats, suggesting that the hypolipidemic effect of probucol may attenuate proteinuria associated with nephrosis. These results suggest that probucol may be a favorable treatment for hyperlipidemia associated with nephrotic syndrome.
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PMID:The lowering effect of probucol on plasma lipoprotein and proteinuria in puromycin aminonucleoside-induced nephrotic rats. 185 87


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