Triglyceride Concentration is Independently Associated with Variation in the LPL Gene in African American and European American Women
Krista Casazza*, 1, Nihal Natour1, Jasmin Divers5, Laura Kelly Vaughan2, Abigail W. Bigham4, Barbara A. Gower1, Gary R. Hunter1, 3, José R. Fernández1, 2
Identifiers and Pagination:Year: 2009
First Page: 23
Last Page: 31
Publisher Id: TOOBESJ-1-23
Article History:Received Date: 21/02/2009
Revision Received Date: 26/03/2009
Acceptance Date: 30/03/2009
Electronic publication date: 28/4/2009
Collection year: 2009
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The regulation of triglyceride (TG) metabolism may be affected by many factors including: race/ethnicity, body composition, body fat distribution, insulin action, and the activity of the lipoprotein lipase (LPL) enzyme. This study was designed to identify the independent effects of body composition, body fat distribution, insulin action, and LPL genetic variation on TG and HDL-C concentration.
The study consisted of premenopausal European American (EA) (n=114) and African American (AA) (n=140) women.
Body composition was measured by dual-energy X-ray absorptiometry (DXA), intra-abdominal adipose tissue (IAAT) by computed tomography (CT), insulin sensitivity (SI) and the acute insulin response to glucose (AIRg) by intravenous glucose tolerance test, median household income by zip-code. An estimate of individual genetic admixture was obtained from the genotyping of 85 ancestry informative markers and used to control for population stratification. Multiple linear regression analyses were used to identify contributions of body composition, IAAT, SI, AIRg, African genetic admixture, and LPL polymorphisms to TG and HDL-C.
AA had lower TG and higher HDL-C than EA. African genetic admixture, IAAT, AIRg, SI, and RS285 were significantly and independently related to TG concentration. SI was the only independent contributor to HDL-C. RS1800590 was not associated with variation in TG or HDL.
Triglyceride concentration appears to be multifactorial in origin and emanates in part from variance in LPL RS285. Future investigations are necessary to understand the mechanisms through which gene polymorphisms, body fat distribution, and insulin action influence the lipid profile.