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Papers In Press, published online ahead of print August 16, 2003
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Institute for Public Health Genetics/Epidemiology, University of Washington, Seattle, WA 98195-7236
Corresponding Author: maustin{at}u.washington.edu
Small, dense low-density lipoproteins (LDL) and hypertriglyceridemia, two highly correlated risk factors, are known to predict for risk of coronary heart disease. Although both LDL size and plasma triglyceride levels are genetically influenced, the molecular basis of LDL heterogeneity and hypertriglyceridemia remain to be established. The objective of this study was to perform a whole genome scan for linkage to LDL size and plasma triglyceride levels in 26 kindreds with familial hypertriglyceridemia (FHTG). LDL size was estimated using gradient gel electrophoresis and genotyping was performed for 355 autosomal markers with an average heterozygosity of 76% and with an average spacing of 10.2 cM. Using variance components linkage analysis, one possible linkage was found for LDL size (LOD = 2.1) on chromosome 6, peak at approximately 140 cM distal to marker F13A1 (1-LOD support interval 116-158, closest marker D6S2436). With adjustment for triglyceride and/or HDL cholesterol, the LOD scores were reduced, but remained in exactly the same chromosomal location. For triglyceride, LOD scores of 2.56 and 2.44 were observed at two locations on chromosome 15, with peaks at approximately 29 and 61 cM distal to marker D15S822 (1-LOD support intervals 30-46 and 48-61, respectively; closest markers D15S643 and D15S211, respectively). These peaks were retained with adjustment for LDL size and/or HDL cholesterol. These findings, if confirmed, suggest that LDL particle size and plasma triglyceride levels could be caused by two different genetic loci in FHTG.
Revised on August 11, 2003
Accepted on August 11, 2003
Genomewide scan for quantitative trait loci influencing low-density lipoprotein size and plasma triglyceride in familial hypertriglyceridemia
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