The Effect of PCSK9 Loss-of-Function Variants on the Postprandial Lipid and ApoB-Lipoprotein Response
Author(s) -
Teik Chye Ooi,
Jacqueline A. Krysa,
Seham Chaker,
Hussein Abujrad,
Janice Mayne,
Kathy Henry,
Marion Cousins,
Angela Raymond,
Colette Favreau,
Monica Taljaard,
Michel Chrètien,
Majambu Mbikay,
Spencer D. Proctor,
Donna F. Vine
Publication year - 2017
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2017-00684
Subject(s) - pcsk9 , postprandial , apolipoprotein b , medicine , endocrinology , ldl receptor , kexin , lipoprotein , proprotein convertase , cholesterol , chemistry , insulin
Proprotein convertase subtilisin kexin 9 (PCSK9) mediates degradation of the low-density lipoprotein receptor (LDLR), thereby increasing plasma low-density lipoprotein cholesterol (LDL-C). Variations in the PCSK9 gene associated with loss of function (LOF) of PCSK9 result in greater expression of hepatic LDLR, lower concentrations of LDL-C, and protection from cardiovascular disease (CVD). Apolipoprotein-B (apoB) remnants also contribute to CVD risk and are similarly cleared by the LDLR. We hypothesized that PCSK9-LOF carriers would have lower fasting and postprandial remnant lipoproteins on top of lower LDL-C.
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