The SCARB1 gene is associated with lipid response to dietary and pharmacological interventions.
The scavenger receptor class B type 1 (SCARB1) gene is a key component in the reverse cholesterol transport pathway and thus plays an important role in lipid metabolism. Studies suggest that the SCARB1 gene may contribute to variation in plasma lipid levels at fasting; however, the results have been inconsistent, and it is unclear whether SCARB1 may also influence lipid response to dietary and pharmacologic interventions. In this study, we examined genetic variation in the SCARB1 gene in participants of the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study for associations with basal lipid levels, changes in lipid measures after dietary fat intake, and fenofibrate treatment. We found that the exon 1 variant SCARB1_G2S was significantly associated with postfenofibrate change for triglycerides (TG) (P = 0.004). Subjects bearing SCARB1_G2S minor allele A tend to have higher responsiveness to fenofibrate in lowering TG. In summary, our study suggested that the SCARB1 gene may serve as a useful marker that predicts variation in baseline lipid levels, postprandial lipid response, and response to fenofibrate intervention.
Liu
Yongjun
Y
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Ordovas
Jose M
JM
Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA.
Gao
Guimin
G
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Province
Michael
M
Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA.
Straka
Robert J
RJ
Experimental and Clinical Pharmacology Department, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA.
Tsai
Michael Y
MY
Laboratory of Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Lai
Chao-Qiang
CQ
Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA.
Zhang
Kui
K
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Borecki
Ingrid
I
Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA.
Hixson
James E
JE
Human Genetics Center, University of Texas Health Science Center, Houston, TX, USA.
Allison
David B
DB
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.|Clinical Nutrition Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Arnett
Donna K
DK
Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, 220E Ryals Public Health Building, 1665 University Blvd., 1530 3rd Avenue South, Birmingham, AL, 35294-0022, USA. arnett@uab.edu.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018955:CD36 Antigens / Q000235:genetics; D004032:Diet; D005260:Female; D011345:Fenofibrate / Q000008:administration & dosage / Q000494:pharmacology*; D005819:Genetic Markers / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D051122:Scavenger Receptors, Class B / Q000235:genetics*
D018955:CD36 Antigens; D005819:Genetic Markers; D000960:Hypolipidemic Agents; D008055:Lipids; C495124:SCARB1 protein, human; D051122:Scavenger Receptors, Class B; D011345:Fenofibrate