Open AccessA regulatory insertion-deletion polymorphism in the FADS gene cluster influences PUFA and lipid profiles among Chinese adults: a population-based study
Author(s) -
Peiqin Li,
Jing Zhao,
Kumar S.D. Kothapalli,
Xiang Li,
Hui Li,
Yuxuan Han,
Shengquan Mi,
Wenhua Zhao,
Qizhai Li,
Hong Zhang,
Yiqing Song,
J. Thomas Brenna,
Ying Gao
Publication year - 2018
Publication title -
american journal of clinical nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.608
H-Index - 336
eISSN - 1938-3207
pISSN - 0002-9165
DOI - 10.1093/ajcn/nqy063
Subject(s) - fads2 , polyunsaturated fatty acid , eicosapentaenoic acid , linoleic acid , docosahexaenoic acid , biology , population , fatty acid , arachidonic acid , blood lipids , alpha linolenic acid , medicine , endocrinology , biochemistry , cholesterol , enzyme , environmental health
Arachidonic acid (AA) is the major polyunsaturated fatty acid (PUFA) substrate for potent eicosanoid signaling to modulate inflammation and thrombosis and is controlled in part by tissue abundance. Fatty acid desaturase 1 (FADS1) catalyzes synthesis of omega-6 (n-3) AA and n-3 eicosapentaenoic acid (EPA). The rs66698963 polymorphism, a 22-base pair (bp) insertion-deletion 137 bp downstream of a sterol regulatory element in FADS2 intron 1, mediates expression of FADS1 in vitro, as well as exerting positive selection in several human populations. The associations between the polymorphism rs66698963 and plasma PUFAs as well as disease phenotypes are unclear.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom