title: Transferability and fine mapping of genome-wide associated loci for lipids in African Americans.
abstract: BACKGROUND
  A recent, large genome-wide association study (GWAS) of European ancestry individuals has identified multiple genetic variants influencing serum lipids. Studies of the transferability of these associations to African Americans remain few, an important limitation given interethnic differences in serum lipids and the disproportionate burden of lipid-associated metabolic diseases among African Americans.
  
  
  METHODS
  We attempted to evaluate the transferability of 95 lipid-associated loci recently identified in European ancestry individuals to 887 non-diabetic, unrelated African Americans from a population-based sample in the Washington, DC area. Additionally, we took advantage of the generally reduced linkage disequilibrium among African ancestry populations in comparison to European ancestry populations to fine-map replicated GWAS signals.
  
  
  RESULTS
  We successfully replicated reported associations for 10 loci (CILP2/SF4, STARD3, LPL, CYP7A1, DOCK7/ANGPTL3, APOE, SORT1, IRS1, CETP, and UBASH3B). Through trans-ethnic fine-mapping, we were able to reduce associated regions around 75% of the loci that replicated.
  
  
  CONCLUSIONS
  Between this study and previous work in African Americans, 40 of the 95 loci reported in a large GWAS of European ancestry individuals also influence lipid levels in African Americans. While there is now evidence that the lipid-influencing role of a number of genetic variants is observed in both European and African ancestry populations, the still considerable lack of concordance highlights the importance of continued ancestry-specific studies to elucidate the genetic underpinnings of these traits.
authors.affiliation: Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. adeyemoa@mail.nih.gov
authors.forename: Adebowale
authors.initials: A
authors.lastname: Adeyemo
authors.forename: Amy R
authors.initials: AR
authors.lastname: Bentley
authors.forename: Katherine G
authors.initials: KG
authors.lastname: Meilleur
authors.forename: Ayo P
authors.initials: AP
authors.lastname: Doumatey
authors.forename: Guanjie
authors.initials: G
authors.lastname: Chen
authors.forename: Jie
authors.initials: J
authors.lastname: Zhou
authors.forename: Daniel
authors.initials: D
authors.lastname: Shriner
authors.forename: Hanxia
authors.initials: H
authors.lastname: Huang
authors.forename: Alan
authors.initials: A
authors.lastname: Herbert
authors.forename: Norman P
authors.initials: NP
authors.lastname: Gerry
authors.forename: Michael F
authors.initials: MF
authors.lastname: Christman
authors.forename: Charles N
authors.initials: CN
authors.lastname: Rotimi
mesh_terms: D001741:Black or African American / Q000235:genetics*; D002318:Cardiovascular Diseases / Q000235:genetics; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D005260:Female; D056426:Genetic Loci; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D005838:Genotype; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D008659:Metabolic Diseases / Q000235:genetics; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D014280:Triglycerides / Q000097:blood*; D044465:White People / Q000235:genetics
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D002784:Cholesterol