Genetic variation at the lipoprotein lipase locus and plasma lipoprotein and insulin levels in the Québec Family Study

التفاصيل البيبلوغرافية
العنوان: Genetic variation at the lipoprotein lipase locus and plasma lipoprotein and insulin levels in the Québec Family Study
المؤلفون: Olavi Ukkola, Jean Bergeron, Jean-Pierre Després, Claude Bouchard, D. C. Rao, Christophe Garenc, Louis Pérusse
المصدر: Atherosclerosis. 158(1)
سنة النشر: 2001
مصطلحات موضوعية: Adult, Male, medicine.medical_specialty, Very low-density lipoprotein, Linkage disequilibrium, Genotype, medicine.medical_treatment, Lipoproteins, Cholesterol, VLDL, HindIII, Lipoproteins, VLDL, Polymerase Chain Reaction, Body Mass Index, chemistry.chemical_compound, High-density lipoprotein, Internal medicine, medicine, Humans, Insulin, Allele, Triglycerides, Genetics, Lipoprotein lipase, Polymorphism, Genetic, Triglyceride, biology, Cholesterol, LDL, Glucose Tolerance Test, Alkadienes, Lipoprotein Lipase, Endocrinology, chemistry, biology.protein, lipids (amino acids, peptides, and proteins), Female, Cardiology and Cardiovascular Medicine
الوصف: The associations between the S447X, BamHI, HindIII and PuII DNA variants of the lipoprotein lipase (LPL) gene and indicators of body fat, fat distribution and plasma lipids and insulin were studied in the Quebec Family Study cohort. Strong linkage disequilibrium among all the markers was observed. For the S447X polymorphism, plasma very low density lipoprotein (VLDL)-cholesterol (chol) (P0.001), total triglyceride (TG) (P= 0.033) and VLDL-TG (P 0.001) levels were lower and high density lipoprotein (HDL)-chol level higher (P0.001) in the subjects homozygous or heterozygous for X447 (X447 + , n =160) compared to the homozygotes for the S447 allele (X447 − , n= 576). The BamHI, PuII and HindIII polymorphisms were not associated with the plasma lipid values when all X447 allele carriers were removed. In addition, the HindIII polymorphism as well as the HindIII and S447X markers combination influenced the insulin area under the curve during an oral glucose tolerance test. We conclude that DNA sequence variation in the LPL gene contributes significantly to the variability in the levels of VLDL-chol, total- and VLDL-TG as well as HDL-chol. The effects of the other polymorphisms considered here are most likely mediated by their linkage disequilibrium with the S447X mutation. In addition, genetic variation at the LPL locus may, by an unknown mechanism, influence insulin metabolism but not body fat variability. © 2001 Elsevier Science Ltd. All rights reserved.
تدمد: 0021-9150
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bda25537d37966b346fae731627a1ec0Test
https://pubmed.ncbi.nlm.nih.gov/11500192Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....bda25537d37966b346fae731627a1ec0
قاعدة البيانات: OpenAIRE