Cardiovascular DiseasesNCT00005214
Epidemiology of Genetic Factors in Lipid Metabolism
An observational study of Cardiovascular Diseases and Heart Diseases, run by The University of Texas Health Science Center, Houston.
Trial summary
To investigate the genetics and epidemiology of fasting and postprandial lipid, lipoprotein, and apolipoprotein levels. Read more about this study
- Who is it for?
- Ages 0 to 100 yearsHealthy volunteers can take part
- Conditions the study is for
- Cardiovascular Diseases, Heart Diseases, Atherosclerosis
- How many people
- Not given
- Where
- No sites listed yet
- Study dates
- Apr 1988to Mar 1993
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 0 to 100 years
- All sexes
- Healthy volunteers accepted
- Child, Adult, Older adult
Study population: Sample of 75 nuclear families from Nancy France. Sample of 100 unrelated Mexican-Americans from Laredo, Texas.
No eligibility criteria
About this study
To investigate the genetics and epidemiology of fasting and postprandial lipid, lipoprotein, and apolipoprotein levels.
Read the detailed description
BACKGROUND:
Altered plasma lipid, lipoprotein, and apolipoprotein levels are associated with the occurrence of coronary heart disease, non-insulin dependent diabetes, and gallbladder disease. Although there are many other environmental and biological correlates, clinical, epidemiological, and experimental lines of evidence indicate that lipid metabolism has a central role in the development of coronary heart disease. Evidence pointing to the association between measures of lipid metabolism and other chronic diseases is no less compelling. Non-insulin dependent diabetes mellitus exhibits both the diagnostic abnormal carbohydrate utilization, and altered lipid metabolism. The hypothesis that abnormal lipid metabolism may be causally involved in gallbladder disease is suggested by the presence of cholesterol saturated bile several years prior to the onset of clinically definable gallstones.
Biometrical genetic studies have established that a significant proportion of the fasting plasma lipid, lipoprotein, and apolipoprotein levels is attributable to genetic differences among individuals. Although these studies indicate that polygenetic variability is contributing, they do not yield information about specific candidate genes whose products are involved in the metabolism of the phenotype of interest. Recent advances in molecular biology enable one to measure genetic variability at candidate loci for several risk factors for the common chronic diseases. With this information the contribution of specific candidate genes to polygenetic and phenotypic variability can be estimated. Estimating the effects of specific candidate loci will facilitate the investigation of the interaction between genetic and environmental factors. This study focussed on restriction fragment length polymorphisms in and around the apolipoprotein B gene and on the apolipoprotein E protein polymorphism. The apolipoprotein B and apolipoprotein E genes were selected because of their central role in lipid metabolism and interaction with dietary factors.
DESIGN NARRATIVE:
Using data and blood samples from the 75 nuclear families of Nancy, a determination was made of the effects of apolipoprotein B and E genes on fasting levels of total cholesterol and triglycerides, LDL-cholesterol, HDL-cholesterol, HDL2-cholesterol, HDL3-cholesterol, apo A-I, apo-B, apo C-III, and apo-E. Genetic variability was directly assessed by DNA restriction site variability in the apolipoprotein B gene and by measuring the apolipoprotein E polymorphism. Data collected from these families permitted the partitioning of the effects of the apolipoprotein B and E genes from the overall polygenetic and phenotypic variance of the measured lipids, lipoproteins, and apolipoproteins.
Fasting and postprandial lipids, lipoproteins, and apolipoproteins were obtained from 100 Mexican-American women. A determination was made of the effects of apolipoprotein E and B genes, disease status, age, and their interactions on fasting and postprandial lipid metabolism.
- Conditions
- Cardiovascular Diseases, Heart Diseases, Atherosclerosis
- Medical subject headings
- Cardiovascular Diseases, Heart Diseases, Atherosclerosis
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 May 2000 (estimated)
- Study startApr 1988
- Study completionMar 1993
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (27)Papers the sponsor has linked to this study.
- Other trials for Cardiovascular DiseasesStudies of the same condition, open and under way.
- More trials run by The University of Texas Health Science Center, HoustonThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case only
- Time perspective
- Cross-sectional
Sponsor and investigators
- Sponsor type
- University, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI)
- Responsible party
- Principal investigator, Eric Boerwinkle, The University of Texas Health Science Center, Houston
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00005214
- Sponsor's protocol ID
- 1093
- Other IDs
- R29HL040613
- Status last verified
- Sep 2021
- First submitted
- 25 May 2000
- Last updated
- 1 Oct 2021
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Surguchov AP, Page GP, Smith L, Patsch W, Boerwinkle E. Polymorphic markers in apolipoprotein C-III gene flanking regions and hypertriglyceridemia. Arterioscler Thromb Vasc Biol. 1996 Aug;16(8):941-7. doi: 10.1161/01.atv.16.8.941.
PubMed 8696957Boerwinkle E, Xiong WJ, Fourest E, Chan L. Rapid typing of tandemly repeated hypervariable loci by the polymerase chain reaction: application to the apolipoprotein B 3' hypervariable region. Proc Natl Acad Sci U S A. 1989 Jan;86(1):212-6. doi: 10.1073/pnas.86.1.212.
PubMed 2911570Boerwinkle E, Chan L. A three codon insertion/deletion polymorphism in the signal peptide region of the human apolipoprotein B (APOB) gene directly typed by the polymerase chain reaction. Nucleic Acids Res. 1989 May 25;17(10):4003. doi: 10.1093/nar/17.10.4003.
PubMed 2567503Gueguen R, Visvikis S, Steinmetz J, Siest G, Boerwinkle E. An analysis of genotype effects and their interactions by using the apolipoprotein E polymorphism and longitudinal data. Am J Hum Genet. 1989 Nov;45(5):793-802.
PubMed 2816943Visvikis S, Chan L, Siest G, Drouin P, Boerwinkle E. An insertion deletion polymorphism in the signal peptide of the human apolipoprotein B gene. Hum Genet. 1990 Mar;84(4):373-5. doi: 10.1007/BF00196239.
PubMed 2307462Seed M, Hoppichler F, Reaveley D, McCarthy S, Thompson GR, Boerwinkle E, Utermann G. Relation of serum lipoprotein(a) concentration and apolipoprotein(a) phenotype to coronary heart disease in patients with familial hypercholesterolemia. N Engl J Med. 1990 May 24;322(21):1494-9. doi: 10.1056/NEJM199005243222104.
PubMed 2139920Boerwinkle E, Lee SS, Butler R, Schumaker VN, Chan L. Rapid typing of apolipoprotein B DNA polymorphisms by DNA amplification. Association between Ag epitopes of human apolipoprotein B-100, a signal peptide insertion/deletion polymorphism, and a 3'flanking DNA variable number of tandem repeats polymorphism of the apolipoprotein B gene. Atherosclerosis. 1990 Apr;81(3):225-32. doi: 10.1016/0021-9150(90)90070-y.
PubMed 1693506Visvikis S, Steinmetz J, Boerwinkle E, Gueguen R, Galteau MM, Siest G. Frequency and effects of the apolipoprotein A-IV polymorphism. Clin Genet. 1990 Jun;37(6):435-41. doi: 10.1111/j.1399-0004.1990.tb03527.x.
PubMed 2383930Boerwinkle E, Visvikis S, Chan L. Two polymorphisms for amino acid substitutions in the APOA4 gene. Nucleic Acids Res. 1990 Aug 25;18(16):4966. doi: 10.1093/nar/18.16.4966. No abstract available.
PubMed 2395672de Temmerman P, Visvikis S, Boerwinkle E, Siest G. Study of the sequence tagged site (STS) in the beginning of human apo A4 gene region. Nucleic Acids Res. 1990 Sep 25;18(18):5576. doi: 10.1093/nar/18.18.5576.
PubMed 2216752Xu CF, Boerwinkle E, Tikkanen MJ, Huttunen JK, Humphries SE, Talmud PJ. Genetic variation at the apolipoprotein gene loci contribute to response of plasma lipids to dietary change. Genet Epidemiol. 1990;7(4):261-75. doi: 10.1002/gepi.1370070405.
PubMed 1977654Boerwinkle E, Hanis CL, Chan L. A unique length polymorphism in the signal peptide region of the apolipoprotein B gene in Mexican-Americans. Nucleic Acids Res. 1990 Dec 11;18(23):7193. doi: 10.1093/nar/18.23.7193.
PubMed 2263508Talmud PJ, Boerwinkle E, Xu CF, Tikkanen MJ, Pietinen P, Huttunen JK, Humphries S. Dietary intake and gene variation influence the response of plasma lipids to dietary intervention. Genet Epidemiol. 1992;9(4):249-60. doi: 10.1002/gepi.1370090404.
PubMed 1356882Shriver MD, Siest G, Boerwinkle E. Length and sequence variation in the apolipoprotein B intron 20 Alu repeat. Genomics. 1992 Oct;14(2):449-54. doi: 10.1016/s0888-7543(05)80240-x.
PubMed 1427859Boerwinkle E, Leffert CC, Lin J, Lackner C, Chiesa G, Hobbs HH. Apolipoprotein(a) gene accounts for greater than 90% of the variation in plasma lipoprotein(a) concentrations. J Clin Invest. 1992 Jul;90(1):52-60. doi: 10.1172/JCI115855.
PubMed 1386087
Study at a glance
From the registry record, last updated by the sponsor on 1 Oct 2021. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Epidemiology of Genetic Factors in Lipid Metabolism
- ClinicalTrials.gov ID
- NCT00005214
- Acronym / sponsor ID
- 1093
- Conditions
- Cardiovascular Diseases, Heart Diseases, Atherosclerosis
- Study type
- Observational
- Recruitment status
- Completed
- Lead sponsor
- The University of Texas Health Science Center, HoustonUniversity, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI)
- Study start
- Apr 1988
- Study completion
- Mar 1993
- First posted
- 26 May 2000 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
To investigate the genetics and epidemiology of fasting and postprandial lipid, lipoprotein, and apolipoprotein levels.
Detailed description
BACKGROUND:
Altered plasma lipid, lipoprotein, and apolipoprotein levels are associated with the occurrence of coronary heart disease, non-insulin dependent diabetes, and gallbladder disease. Although there are many other environmental and biological correlates, clinical, epidemiological, and experimental lines of evidence indicate that lipid metabolism has a central role in the development of coronary heart disease. Evidence pointing to the association between measures of lipid metabolism and other chronic diseases is no less compelling. Non-insulin dependent diabetes mellitus exhibits both the diagnostic abnormal carbohydrate utilization, and altered lipid metabolism. The hypothesis that abnormal lipid metabolism may be causally involved in gallbladder disease is suggested by the presence of cholesterol saturated bile several years prior to the onset of clinically definable gallstones.
Biometrical genetic studies have established that a significant proportion of the fasting plasma lipid, lipoprotein, and apolipoprotein levels is attributable to genetic differences among individuals. Although these studies indicate that polygenetic variability is contributing, they do not yield information about specific candidate genes whose products are involved in the metabolism of the phenotype of interest. Recent advances in molecular biology enable one to measure genetic variability at candidate loci for several risk factors for the common chronic diseases. With this information the contribution of specific candidate genes to polygenetic and phenotypic variability can be estimated. Estimating the effects of specific candidate loci will facilitate the investigation of the interaction between genetic and environmental factors. This study focussed on restriction fragment length polymorphisms in and around the apolipoprotein B gene and on the apolipoprotein E protein polymorphism. The apolipoprotein B and apolipoprotein E genes were selected because of their central role in lipid metabolism and interaction with dietary factors.
DESIGN NARRATIVE:
Using data and blood samples from the 75 nuclear families of Nancy, a determination was made of the effects of apolipoprotein B and E genes on fasting levels of total cholesterol and triglycerides, LDL-cholesterol, HDL-cholesterol, HDL2-cholesterol, HDL3-cholesterol, apo A-I, apo-B, apo C-III, and apo-E. Genetic variability was directly assessed by DNA restriction site variability in the apolipoprotein B gene and by measuring the apolipoprotein E polymorphism. Data collected from these families permitted the partitioning of the effects of the apolipoprotein B and E genes from the overall polygenetic and phenotypic variance of the measured lipids, lipoproteins, and apolipoproteins.
Fasting and postprandial lipids, lipoproteins, and apolipoproteins were obtained from 100 Mexican-American women. A determination was made of the effects of apolipoprotein E and B genes, disease status, age, and their interactions on fasting and postprandial lipid metabolism.
Study design
- Observational model
- Case only
- Time perspective
- Cross-sectional
Who may qualify
- Ages
- 0 to 100 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Sample of 75 nuclear families from Nancy France. Sample of 100 unrelated Mexican-Americans from Laredo, Texas.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 1 Oct 2021.
- Background: PubMed 8696957Surguchov AP, Page GP, Smith L, Patsch W, Boerwinkle E. Polymorphic markers in apolipoprotein C-III gene flanking regions and hypertriglyceridemia. Arterioscler Thromb Vasc Biol. 1996 Aug;16(8):941-7. doi: 10.1161/01.atv.16.8.941.
- Background: PubMed 2911570Boerwinkle E, Xiong WJ, Fourest E, Chan L. Rapid typing of tandemly repeated hypervariable loci by the polymerase chain reaction: application to the apolipoprotein B 3' hypervariable region. Proc Natl Acad Sci U S A. 1989 Jan;86(1):212-6. doi: 10.1073/pnas.86.1.212.
- Background: PubMed 2567503Boerwinkle E, Chan L. A three codon insertion/deletion polymorphism in the signal peptide region of the human apolipoprotein B (APOB) gene directly typed by the polymerase chain reaction. Nucleic Acids Res. 1989 May 25;17(10):4003. doi: 10.1093/nar/17.10.4003.
- Background: PubMed 2816943Gueguen R, Visvikis S, Steinmetz J, Siest G, Boerwinkle E. An analysis of genotype effects and their interactions by using the apolipoprotein E polymorphism and longitudinal data. Am J Hum Genet. 1989 Nov;45(5):793-802.
- Background: PubMed 2307462Visvikis S, Chan L, Siest G, Drouin P, Boerwinkle E. An insertion deletion polymorphism in the signal peptide of the human apolipoprotein B gene. Hum Genet. 1990 Mar;84(4):373-5. doi: 10.1007/BF00196239.
- Background: PubMed 2139920Seed M, Hoppichler F, Reaveley D, McCarthy S, Thompson GR, Boerwinkle E, Utermann G. Relation of serum lipoprotein(a) concentration and apolipoprotein(a) phenotype to coronary heart disease in patients with familial hypercholesterolemia. N Engl J Med. 1990 May 24;322(21):1494-9. doi: 10.1056/NEJM199005243222104.
- Background: PubMed 1693506Boerwinkle E, Lee SS, Butler R, Schumaker VN, Chan L. Rapid typing of apolipoprotein B DNA polymorphisms by DNA amplification. Association between Ag epitopes of human apolipoprotein B-100, a signal peptide insertion/deletion polymorphism, and a 3'flanking DNA variable number of tandem repeats polymorphism of the apolipoprotein B gene. Atherosclerosis. 1990 Apr;81(3):225-32. doi: 10.1016/0021-9150(90)90070-y.
- Background: PubMed 2383930Visvikis S, Steinmetz J, Boerwinkle E, Gueguen R, Galteau MM, Siest G. Frequency and effects of the apolipoprotein A-IV polymorphism. Clin Genet. 1990 Jun;37(6):435-41. doi: 10.1111/j.1399-0004.1990.tb03527.x.
- Background: PubMed 2395672Boerwinkle E, Visvikis S, Chan L. Two polymorphisms for amino acid substitutions in the APOA4 gene. Nucleic Acids Res. 1990 Aug 25;18(16):4966. doi: 10.1093/nar/18.16.4966. No abstract available.
- Background: PubMed 2216752de Temmerman P, Visvikis S, Boerwinkle E, Siest G. Study of the sequence tagged site (STS) in the beginning of human apo A4 gene region. Nucleic Acids Res. 1990 Sep 25;18(18):5576. doi: 10.1093/nar/18.18.5576.
- Background: PubMed 1977654Xu CF, Boerwinkle E, Tikkanen MJ, Huttunen JK, Humphries SE, Talmud PJ. Genetic variation at the apolipoprotein gene loci contribute to response of plasma lipids to dietary change. Genet Epidemiol. 1990;7(4):261-75. doi: 10.1002/gepi.1370070405.
- Background: PubMed 2263508Boerwinkle E, Hanis CL, Chan L. A unique length polymorphism in the signal peptide region of the apolipoprotein B gene in Mexican-Americans. Nucleic Acids Res. 1990 Dec 11;18(23):7193. doi: 10.1093/nar/18.23.7193.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
Questions about this trial
What is this clinical trial studying?
An observational study of Cardiovascular Diseases and Heart Diseases, run by The University of Texas Health Science Center, Houston.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 1 Oct 2021. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00005214, which also lists 27 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 1 Oct 2021.