Journal
SCIENCE
Volume 322, Issue 5908, Pages 1702-1705Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1161524
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Funding
- NIH [R01 HL088119, R01 AR046838, U01 HL72515, R01 AG18728, U01 HL084756]
- General Clinical Research Centers Program
- National Center for Research Resources
- University of Maryland General Clinical Research Center [M01 RR 16500]
- University of Maryland Clinical Nutrition Research Unit [P30 DK072488]
- Johns Hopkins University General Clinical Research Center [M01 RR 000052]
- Baltimore Veterans Administration Geriatric Research and Education Clinical Center
- Paul Beeson Faculty Scholars in Aging Program
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Apolipoprotein C-III ( apoC-III) inhibits triglyceride hydrolysis and has been implicated in coronary artery disease. Through a genome- wide association study, we have found that about 5% of the Lancaster Amish are heterozygous carriers of a null mutation ( R19X) in the gene encoding apoC- III ( APOC3) and, as a result, express half the amount of apoC- III present in noncarriers. Mutation carriers compared with noncarriers had lower fasting and postprandial serum triglycerides, higher levels of HDL- cholesterol and lower levels of LDL- cholesterol. Subclinical atherosclerosis, as measured by coronary artery calcification, was less common in carriers than noncarriers, which suggests that lifelong deficiency of apoC- III has a cardioprotective effect.
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