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.
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Yongjun
Y
Liu
Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA.
Jose M
JM
Ordovas
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Guimin
G
Gao
Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA.
Michael
M
Province
Experimental and Clinical Pharmacology Department, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA.
Robert J
RJ
Straka
Laboratory of Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Michael Y
MY
Tsai
Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA, USA.
Chao-Qiang
CQ
Lai
Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Kui
K
Zhang
Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA.
Ingrid
I
Borecki
Human Genetics Center, University of Texas Health Science Center, Houston, TX, USA.
James E
JE
Hixson
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.
David B
DB
Allison
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.
Donna K
DK
Arnett
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