Publications by authors named "Weisweiler P"

The effects of fluvastatin and bezafibrate on lipids, lipoproteins, and apoproteins (apo) were investigated in a multicenter randomized, double-blind, parallel-group study. After 8 weeks of strictly controlled (computer-based assessment) dietary stabilization, patients with primary hypercholesterolemia (low-density lipoprotein cholesterol [LDL-C] > or = 160 mg/dL; triglycerides < or = 300 mg/dL) were enrolled into a 6-week placebo phase. Altogether, 131 patients were randomized to receive either fluvastatin at 40 mg once daily (n = 64; mean age 53 years) or bezafibrate at 400 mg once daily (n = 67; mean age 52 years) for 12 weeks.

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Effects on plasma lipoproteins, lecithin:cholesterol acyltransferase (LCAT), and postheparin lipase (LPL and HTGL) activities were studied in 18 patients with familial hypercholesterolemia during 8-week treatment periods with colestipol (15 g/d), fenofibrate (0.25 g/d), and colestipol plus fenofibrate. Lipoprotein lipids and apolipoproteins were determined by standard procedures, LCAT by a self-substrate method, and lipases by nonradioisotopic methods.

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29 patients with primary hypercholesterolemia were treated for 8 weeks each with either bezafibrate (200 mg t.i.d.

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Sixteen subjects with familial hypercholesterolaemia were randomly assigned to treatment with simvastatin 20-40 mg/day (an inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase) or with bezafibrate 600 mg/day (a clofibrate analogue) for 12 weeks. Both drugs produced significant reductions in serum and LDL cholesterol; mean percentage fall -30.5% and -38.

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Apolipoproteins (Apo) A-I and A-II from human high-density lipoproteins (HDL) were isolated and quantified by fast-protein liquid chromatography using a Superose 12 column (gel filtration) followed by a Mono Q column (anion-exchanger). The separation times were 45 min and 15 min, respectively. Identities of both apolipoproteins were confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and by double immunodiffusion.

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Plasma lipoprotein concentrations and post-heparin lipoprotein lipase, hepatic triglyceride lipase (HTGL), and lecithin:cholesterol acyltransferase (LCAT) activities were determined in 10 obese women before and after weight loss. In period I, a diet was given to maintain constant weight for 3 weeks. In period II, total calories were restricted to 600 kilocalories/day for 3 weeks.

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The mechanism leading to hyperlipidemia in the nephrotic syndrome is not fully understood but may be related in part to loss of high density lipoproteins in the urine of patients with nephrosis. To prove this hypothesis, we compared serum lipoprotein profiles with the excretion of high density lipoproteins in urine in 19 nephrotic patients. Serum cholesterol ranged from 19-152 (median value 45) mg/dl in very low density lipoproteins (VLDL), from 130-443 (median 186) mg/dl in low density lipoproteins (LDL) and from 19-64 (median 33) mg/dl in high density lipoproteins (HDL).

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The influence of hydrochlorothiazide and atenolol on serum lipoproteins was investigated in a randomized, prospective study on 68 men with essential hypertension. Cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDH) cholesterol, triglycerides, and the apolipoproteins AI and B were followed up to 42 months after starting therapy. Following atenolol serum (HDL) cholesterol decreased and serum triglycerides increased significantly (p less than 0.

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Serum lipoprotein lipids and apolipoproteins A-I, B, and E were investigated in Type 1 (insulin-dependent) diabetics, Type 2 (non-insulin-dependent) diabetics, and two control groups, twenty subjects each. Lipoproteins were separated and analysed by common methods, apolipoproteins were measured by endpoint immunonephelometry. Compared with controls, Type 2 diabetics had increased serum apolipoprotein E levels (0.

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Apolipoprotein B has previously been thought to be a homogeneous protein. Recently, it has been shown by SDS polyacrylamide gel electrophoresis that it consists of several species with different molecular weights. The present paper reports the separation of very low density lipoprotein (VLDL) and chylomicron derived apolipoprotein B by high performance gel permeation chromatography in SDS.

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We investigated effects of fat saturation and fat restriction on very low-density apolipoproteins (VLDL) including the isoforms. Normolipidemic women (22) were given a reference diet, a polyunsaturated diet, and a low-fat, polyunsaturated diet for 6 wk each. The polyunsaturated diet decreased cholesterol and apolipoprotein B levels in VLDL (-33.

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Using "high-performance" anion-exchange chromatography, we isolated and quantified human C apolipoproteins (apo C) from very-low-density lipoproteins (VLDL) in serum. As revealed by isoelectric focusing and double immunodiffusion against monospecific antisera, apo C-I, apo C-II, apo C-III0, apo C-III1, and apo C-III2 were purified to homogeneity. Assay reproducibility (coefficients of variation) ranged between 0.

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Using fast protein chromatofocusing, a high-efficiency column chromatography method with a self-generated pH gradient and focusing effects, soluble human very-low-density lipoprotein (VLDL) apolipoproteins were fractionated between pH 6.3 and 4.0.

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Effects on serum lipoproteins were studied in ten patients with familial hypercholesterolaemia (FH) during consecutive eight-week treatment periods with fenofibrate 0.3 g/day, fenofibrate plus colestipol, 15 g/day, and fenofibrate 0.25 g/day plus colestipol.

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This study was designed to determine the effects of polyunsaturated fats and of reducing intake of total fat on serum lipids, lipoproteins, and apolipoproteins. Twenty-two normolipidemic women living in a nunnery were given a reference diet (fat/carbohydrate 42/46% of energy, P/S ratio 0.16), a polyunsaturated diet (42/46%, P/S 1,0), and a low-fat, polyunsaturated diet (32/56%, P/S 1.

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The effects on serum lipoproteins were studied in 8 patients with familial heterozygous hypercholesterolemia and 9 patients with familial combined hyperlipidemia during an 8-week treatment with fenofibrate. VLDL, IDL, LDL and HDL were isolated by ultracentrifugation and precipitation. Lipids and apolipoproteins A-I and B were determined by enzymatic and immunonephelometric techniques, respectively.

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We studied the effect on the serum LCAT activity and apolipoproteins in ten subjects with primary hypercholesterolemia after treatment with beta-sitosterol. The 2-month administration of beta-sitosterol resulted in an increase of the fractional as well as of the molar esterification rate of the LCAT. These alterations were associated with a decrease of the levels of total, esterified, and unesterified cholesterol, whereas the levels of HDL-cholesterol and the apolipoproteins A-I and B were not affected.

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A laser immunonephelometric procedure for the determination of human apolipoproteins A-I, B, and E in serum and lipoproteins was developed. Coefficients of variation were 2.3%-3.

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Since VLDL and LDL are involved in atherogenesis, their response to dietary modification was studied in 15 normal male prisoners. A 3-month reference diet (P/S ratio 0.3, daily cholesterol intake 370 mg) was compared with a modified fat diet (P/S 1.

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