Trial reportAtherosclerosis1999
Metabolic basis of high density lipoproteins and apolipoprotein A-I increase by HMG-CoA reductase inhibition in healthy subjects and a patient with coronary artery disease.
Trial report in Atherosclerosis, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00458055 (Treatment Study for Severe High-Density Lipoprotein Deficiency), which is not on this map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Treatment Study for Severe High-Density Lipoprotein Deficiency
Open the trial in the graphWho cites it
17 citing papers in PubMed.
- Rosuvastatin 20 mg restores normal HDL-apoA-I kinetics in type 2 diabetes.Journal of lipid research · 2009Trial
- Cellular cholesterol efflux to plasma from moderately hypercholesterolaemic type 1 diabetic patients is enhanced, and is unaffected by simvastatin treatment.Diabetologia · 2005Trial
- Association Between High-Density Lipoprotein Cholesterol Levels and Prognoses in Patients With Stroke.Journal of the American Heart Association · 2026Observational
- Effect of fasting and feeding on apolipoprotein A-I kinetics in preβScientific reports · 2020Article
- Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Role of HDL in those with diabetes.Current cardiology reports · 2014Review
- Plasma apolipoprotein A1 as a biomarker for Parkinson disease.Annals of neurology · 2013Article
- Review
- Raising HDL cholesterol in women.International journal of women's health · 2010Article
- Cholesteryl ester transfer protein: at the heart of the action of lipid-modulating therapy with statins, fibrates, niacin, and cholesteryl ester transfer protein inhibitors.European heart journal · 2010Review
- Vasculoprotective Effects of Apolipoprotein Mimetic Peptides: An Evolving Paradigm In Hdl Therapy (Vascular Disease Prevention, In Press.).Vascular disease prevention · 2009Article
- HDL therapy for cardiovascular diseases: the road to HDL mimetics.Current atherosclerosis reports · 2008Review
- Simvastatin reverses the hypertension of heterozygous mice lacking cystathionine beta-synthase and apolipoprotein A-I.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- High density lipoprotein cholesterol: an evolving target of therapy in the management of cardiovascular disease.Vascular health and risk management · 2008Review
- Anti-inflammatory effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy.Diabetologia · 2007Article
- Studying apolipoprotein turnover with stable isotope tracers: correct analysis is by modeling enrichments.Journal of lipid research · 2006Review
- Statin-induced inhibition of the Rho-signaling pathway activates PPARalpha and induces HDL apoA-I.The Journal of clinical investigation · 2001Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HMG-CoA reductase inhibitors, such as pravastatin, are widely used as lipid lowering drugs in hypercholesterolemia. Pravastatin does not only reduce the atherogenic low density lipoprotein (LDL)-cholesterol, but is also increasing high density lipoprotein (HDL)-cholesterol. However, the mechanism leading to an increase of HDL are unclear. Therefore, the effects of pravastatin on the in vivo kinetics of apolipoprotein (apo) A-I were studied in six normolipidemic subjects and in a patient with coronary artery disease (CAD) utilizing stable isotope tracer techniques. Two turnover studies were performed. The first turnover study was carried out before any drug treatment, the second study after 6 weeks of 40 mg pravastatin/day. Three times deuterium labeled L-leucine (3D-leucine) was given as a primed bolus constant infusion (bolus: 1340 microg/kg; infusion: 22 microg/kg per h), and tracer uptake into HDL apoA-I was determined by gas chromatography (GC)-mass-spectrometry (MS). In the healthy subjects HDL-cholesterol increased by 13% and apoA-I increased by 12% under pravastatin treatment. The HDL in the CAD patient decreased by 3% and apoA-I increased by 2%. Prior to drug treatment the mean apoA-I fractional synthetic rate (FSR) was 0.194 per day (S.D. +/- 0.02) and apoA-I production rate (PR) was 10.8 mg/kg per day (S.D. +/- 2.1). The CAD patient had a FSR of 0.219 per day and a PR of 10.6 mg/kg per day. After treatment with pravastatin the mean apoA-I FSR was 0.204 per day (S.D. +/- 0.02) and apoA-I PR was 12.5 mg/kg per day (S.D. +/- 1.5) in the healthy subjects. Despite only minor changes of HDL and apoA-I in the CAD patient, there were significant changes of FSR (0.267 per day) and PR (13.1 mg/kg per day) with pravastatin treatment. The in vivo kinetic data demonstrate an increased FSR of apoA-I. The increase in apoA-I is due to an increased PR of apoA-I. This study demonstrates increased production of HDL apoA-I as the metabolic cause of the increase in HDL and apoA-I levels under inhibition of HMG-CoA reductase in man.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.