Document Detail


Hepatic lipase gene -514C>T variant is associated with exercise training-induced changes in VLDL and HDL by lipoprotein lipase.
MedLine Citation:
PMID:  21960661     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Our objective was to test the hypothesis that a common polymorphism in the hepatic lipase (HL) gene (LIPC -514C>T, rs1800588) influences aerobic exercise training-induced changes in TG, very-low-density lipoprotein (VLDL), and high-density lipoprotein (HDL) through genotype-specific increases in lipoprotein lipase (LPL) activity and that sex may affect these responses. Seventy-six sedentary overweight to obese men and women aged 50-75 yr at risk for coronary heart disease (CHD) underwent a 24-wk prospective study of the LIPC -514 genotype-specific effects of exercise training on lipoproteins measured enzymatically and by nuclear magnetic resonance, postheparin LPL and HL activities, body composition by dual energy x-ray absorptiometry and computer tomography scan, and aerobic capacity. CT genotype subjects had higher baseline total cholesterol, HDL-C, HDL(2)-C, large HDL, HDL particle size, and large LDL than CC homozygotes. Exercise training elicited genotype-specific decreases in VLDL-TG (-22 vs. +7%; P < 0.05; CC vs. CT, respectively), total VLDL and medium VLDL, and increases in HDL-C (7 vs. 4%; P < 0.03) and HDL(3)-C with significant genotype×sex interactions for the changes in HDL-C and HDL(3)-C (P values = 0.01-0.02). There were also genotype-specific changes in LPL (+23 vs. -6%; P < 0.05) and HL (+7 vs. -24%; P < 0.01) activities, with LPL increasing only in CC subjects (P < 0.006) and HL decreasing only in CT subjects (P < 0.007). Reductions in TG, VLDL-TG, large VLDL, and medium VLDL and increases in HDL(3)-C and small HDL particles correlated significantly with changes in LPL, but not HL, activity only in CC subjects. This suggests that the LIPC -514C>T variant significantly affects training-induced anti-atherogenic changes in VLDL-TG, VLDL particles, and HDL through an association with increased LPL activity in CC subjects, which could guide therapeutic strategies to reduce CHD risk.
Authors:
Tina E Brinkley; Amy Halverstadt; Dana A Phares; Robert E Ferrell; Ronald L Prigeon; James M Hagberg; Andrew P Goldberg
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-29
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  111     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-14     Completed Date:  2012-04-30     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1871-6     Citation Subset:  IM    
Affiliation:
Dept. of Kinesiology, Univ. of Maryland, College Park, MD 20742-2611, USA.
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MeSH Terms
Descriptor/Qualifier:
Aged
Base Sequence
Coronary Disease / genetics,  metabolism,  prevention & control
DNA Primers / genetics
Exercise Therapy*
Female
Genetic Association Studies
Humans
Lipase / genetics*
Lipoprotein Lipase / metabolism*
Lipoproteins, HDL / blood*
Lipoproteins, VLDL / blood*
Male
Middle Aged
Polymorphism, Single Nucleotide*
Prospective Studies
Risk Factors
Sedentary Lifestyle
Triglycerides / blood
Grant Support
ID/Acronym/Agency:
AG-00268/AG/NIA NIH HHS; AG-15389/AG/NIA NIH HHS; AG-17474/AG/NIA NIH HHS; AG-18408/AG/NIA NIH HHS; AG-20116/AG/NIA NIH HHS; DK-46204/DK/NIDDK NIH HHS; P30 AG-028747/AG/NIA NIH HHS; P30 DK-072488/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/DNA Primers; 0/Lipoproteins, HDL; 0/Lipoproteins, VLDL; 0/Triglycerides; 0/very low density lipoprotein triglyceride; EC 3.1.1.3/Lipase; EC 3.1.1.3/hepatic lipase, human; EC 3.1.1.34/LPL protein, human; EC 3.1.1.34/Lipoprotein Lipase
Comments/Corrections

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