Objective: To test the hypothesis that variations in serum insulin concentrations and insulin action may influence serum concentrations of lipoprotein(a) [Lp(a)].
Research Design And Methods: A cross-sectional analysis of fasting serum insulin and Lp(a) concentrations were conducted in a group of 54 healthy adult men 23-61 years of age. Measures of dietary intake, exercise, smoking, alcohol ingestion, body mass index (BMI), fasting plasma lipoprotein lipid concentrations, and serum sex hormone and fasting glucose levels were also determined.
We have examined the influence of simvastatin, a competitive inhibitor of 3-hydroxy-3-methyl glutaryl coenzyme A reductase on plasma concentrations of lipids and lipoproteins, the rates of cholesterol biosynthesis and degradation of 125I-labelled LDL by freshly isolated mononuclear leucocytes and the 24 h urinary excretion of mevalonic acid in patients with heterozygous familial hypercholesterolaemia. Patients were treated with progressively increasing doses of simvastatin (20, 40, and 80 mg day-1) taken in a twice-daily dosage for a period of 6 weeks on each dose. Plasma concentrations of LDL cholesterol decreased by 36.
View Article and Find Full Text PDFWe evaluated the effects of different doses of lovastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG CoA reductase) and the rate-limiting enzyme in cholesterol biosynthesis, on parameters of cholesterol homeostasis in freshly isolated mononuclear leukocytes from 19 patients with heterozygous familial hypercholesterolemia. Patients were treated with sequentially increasing doses of lovastatin (10 to 80 mg/day in a twice-daily regimen). The in vitro activity of HMG CoA reductase and cholesterol synthesis from 2-14C-acetate was determined in mononuclear cells obtained under steady-state conditions after patients had spent 6 weeks on doses of 20, 40, or 80 mg/day.
View Article and Find Full Text PDFIn normal humans low density lipoproteins (LDL) constitute the major lipoprotein responsible for the delivery of cholesterol to cells and their uptake results in a decrease in cholesterol biosynthesis and an increase in cholesterol esterification. In the present study, we have examined whether plasma lipoproteins from patients with abetalipoproteinemia (ABL), who lack LDL in their plasma, can stimulate intracellular cholesterol esterification and, quantitatively, how this compares with normal LDL. Fibroblasts from normal and abetalipoproteinemic patients had similar cholesterol esterification rates when LDL was present in the medium.
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