In:
Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 18, No. 7 ( 1998-07), p. 1061-1068
Abstract:
Abstract —We explored the genetic control of cholesterolemic responses to dietary cholesterol and fat in 575 pedigreed baboons. We measured cholesterol in β-lipoproteins (low density lipoprotein cholesterol [LDLC]) in blood drawn from baboons while they were consuming a baseline (low in cholesterol and fat) diet, a high–saturated fat (lard) diet, and a high-cholesterol, high–saturated fat diet. In addition to baseline levels (LDLC Base ), we analyzed two variables for diet response: LDLC RF , which represents the LDLC response to increasing dietary fat (ie, high-fat diet minus baseline), and LDLC RC , which represents the LDLC response to increasing dietary cholesterol level (ie, high-cholesterol, high-fat diet minus high-fat diet). Heritabilities ( h 2 ) of the 3 traits were 0.59 for LDLC Base , 0.14 for LDLC RF , and 0.59 for LDLC RC . In addition, LDLC Base and LDLC RC had a significant genetic correlation (ie, ρ G =0.54), suggesting that 1 or more genes exert pleiotropic effects on the 2 traits. Segregation analyses detected a single major locus that accounted for nearly all genetic variation in LDLC RC and some genetic variation in LDLC Base and LDLC RF and confirmed the presence of a different major locus that influences LDLC Base alone. Preliminary linkage analyses indicated that neither locus was linked to the LDL receptor gene, a likely candidate locus for LDLC. Detection of these major loci with large effects on the LDLC response to dietary cholesterol in a nonhuman primate offers hope of detecting and ultimately identifying similar loci that determine LDLC variation in human populations.
Type of Medium:
Online Resource
ISSN:
1079-5642
,
1524-4636
DOI:
10.1161/01.ATV.18.7.1061
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1998
detail.hit.zdb_id:
1494427-3
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