» Articles » PMID: 16416313

Variation in the Lipoprotein Lipase Gene Influences Exercise-induced Left Ventricular Growth

Overview
Specialty General Medicine
Date 2006 Jan 18
PMID 16416313
Citations 3
Authors
Affiliations
Soon will be listed here.
Abstract

The adult heart relies predominantly on fatty acids (FA) for energy generation, and defects in FA catabolism cause dramatic left ventricular (LV) growth in early age. Since lipoprotein lipase (LPL) is the key enzyme in plasma triglyceride catabolism and is highly expressed in the myocardium, we investigated an association between the functional LPL gene serine 447 stop (S447X) variant and exercise-induced LV growth. The S447X variant was genotyped in 146 British Army recruits undergoing a 10-week exercise programme. Over the training period, X447 allele carriers showed less LV growth than S447 homozygotes (SS, 5.8+/-0.7%; SX, 2.2+/-1.5%; P=0.03) and a decrease in systolic blood pressure (DeltaSBP: SS, 1.9+/-1.3 mmHg; SX, -5.7+/-2.2 mmHg; P=0.015). Although LPL genotype did not significantly predict LV growth with DeltaSBP in statistical modelling (LPL, P=0.14; DeltaSBP, P=0.06), regression analysis indicated that LPL S447X genotype effect on DeltaSBP accounted for only 20% of the effect on LV growth. In multivariate analysis, LPL, peroxisome-proliferator-activated receptor alpha and angiotensin-converting enzyme genotypes were independent predictors of cardiac growth. Thus, LPL S447X genotype influenced exercise-induced changes in LV mass and SBP. Change in blood pressure accounted for a proportion of LV growth. These data suggest that increased myocardial FA availability may reduce exercise-induced LV growth.

Citing Articles

Deep-targeted sequencing of endothelial nitric oxide synthase gene exons uncovers exercise intensity and ethnicity-dependent associations with post-exercise hypotension.

Pescatello L, Schifano E, Ash G, Panza G, Corso L, Chen M Physiol Rep. 2017; 5(22).

PMID: 29180482 PMC: 5704084. DOI: 10.14814/phy2.13510.


DGAT1 expression increases heart triglyceride content but ameliorates lipotoxicity.

Liu L, Shi X, Bharadwaj K, Ikeda S, Yamashita H, Yagyu H J Biol Chem. 2009; 284(52):36312-36323.

PMID: 19778901 PMC: 2794747. DOI: 10.1074/jbc.M109.049817.


Lipoprotein lipase and heart size.

Luft F J Mol Med (Berl). 2006; 84(2):109-11.

PMID: 16416314 DOI: 10.1007/s00109-005-0018-0.

References
1.
Brull D, Dhamrait S, Myerson S, Erdmann J, Woods D, World M . Bradykinin B2BKR receptor polymorphism and left-ventricular growth response. Lancet. 2001; 358(9288):1155-6. DOI: 10.1016/s0140-6736(01)06273-0. View

2.
Vaziri N, Liang K, Barton C . Effect of increased afterload on cardiac lipoprotein lipase and VLDL receptor expression. Biochim Biophys Acta. 1999; 1436(3):577-84. DOI: 10.1016/s0005-2760(98)00170-2. View

3.
Humphries S, Nicaud V, Margalef J, Tiret L, Talmud P . Lipoprotein lipase gene variation is associated with a paternal history of premature coronary artery disease and fasting and postprandial plasma triglycerides: the European Atherosclerosis Research Study (EARS). Arterioscler Thromb Vasc Biol. 1998; 18(4):526-34. DOI: 10.1161/01.atv.18.4.526. View

4.
Masuzaki H, Jingami H, Matsuoka N, Nakagawa O, Ogawa Y, Mizuno M . Regulation of very-low-density lipoprotein receptor in hypertrophic rat heart. Circ Res. 1996; 78(1):8-14. DOI: 10.1161/01.res.78.1.8. View

5.
Rupp H, Zarain-Herzberg A, Maisch B . The use of partial fatty acid oxidation inhibitors for metabolic therapy of angina pectoris and heart failure. Herz. 2002; 27(7):621-36. DOI: 10.1007/s00059-002-2428-x. View