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PPARα L162V polymorphism alters the potential of n‐3 fatty acids to increase lipoprotein lipase activity
Author(s) -
Rudkowska Iwona,
CaronDorval Dominique,
Verreault Mélanie,
Couture Patrick,
Deshaies Yves,
Barbier Olivier,
Vohl MarieClaude
Publication year - 2010
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200900085
Subject(s) - lipoprotein lipase , lipase , polymorphism (computer science) , chemistry , hepatic lipase , biochemistry , biology , enzyme , gene , allele
Omega‐3 fatty acids (FAs) may accelerate plasma triglyceride (TG) clearance by altering lipoprotein lipase (LPL) activity. Yet, the ability of n‐3 FAs to increase LPL activity is dependent on transcription factors such as peroxisome proliferator‐activated receptor alpha (PPARα). The objective was to examine the effects of n‐3 FAs on LPL activity considering the occurrence of PPAR α L162V polymorphism. First, 14 pairs of men either L162 homozygotes or carriers of the V162 allele were supplemented with n‐3 FAs. Second, transient transfections in HepG2 cells, for the L162‐ and V162‐PPARα variants with the peroxisome proliferator‐response element from the human LPL gene, were transactivated with n‐3 FAs. In vivo results demonstrate that the LPL activity increased non‐significantly by 14.4% in L162 homozygotes compared with 6.6% in carriers of the PPAR α‐V162 allele, after n‐3 FA supplementation. Additionally, the L162 homozygotes tended towards an inverse correlation between LPL activities and plasma TG levels. Conversely, carriers of the V162 allele showed no such relationship. In vitro data demonstrates that transcription rates of LPL tended to be higher for the L162‐PPARα than V162‐PPARα after n‐3 FAs activation. Overall, these results indicate that n‐3 FA supplementation increases the transcription rate of LPL to a greater extent in L162‐PPARα than V162‐PPARα.