2006
DOI: 10.1016/j.metabol.2006.07.018
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Longitudinal analysis of haplotypes and polymorphisms of the APOA5 and APOC3 genes associated with variation in serum triglyceride levels: the Bogalusa Heart Study

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Cited by 33 publications
(34 citation statements)
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“…In this study, the TG levels did not differ between the genotypes of the APOC3 3238C>G SNP, which is inconsistent with results of previous studies in a Tehranian and an Indian population [24,32]; other studies have indicated that this association was found to be either independent of other polymorphisms in the APOC3/APOA5 region [33] or dependent on them [34]. …”
Section: Discussioncontrasting
confidence: 99%
“…In this study, the TG levels did not differ between the genotypes of the APOC3 3238C>G SNP, which is inconsistent with results of previous studies in a Tehranian and an Indian population [24,32]; other studies have indicated that this association was found to be either independent of other polymorphisms in the APOC3/APOA5 region [33] or dependent on them [34]. …”
Section: Discussioncontrasting
confidence: 99%
“…Based on population-based studies, there is an association between the level of TG and the ApoAI-CIII-AIV gene cluster in individuals with hyper triglyceridemia [5]. Increasing the level of TG is a major independent risk factor for CAD across populations from America [6,7], Europe [8,9], and Asia [10,11]. In addition, there are other studies assessing the association between ApoE and ApoB gene polymorphisms with lipid levels in Iranians [12], and they show that this population has an inherent tendency for dyslipidemia associated with high risk of CAD [12,13].…”
Section: Introductionmentioning
confidence: 99%
“…19 Among these, APOCIII and the recently identified APOA5 genes have a regulatory role in triglyceride metabolism. [20][21][22] APOA5 influences the triglyceride metabolism by 2 possible mechanisms: (1) enhancing intravascular triglyceride hydrolysis by activating the lipoprotein lipase, and (2) decreasing the serum concentration of triglycerides through inhibition of hepatic very-low-density lipoprotein-triglyceride production. 23,24 Polymorphisms of APOA5 can influence the function of the protein transcript, which can modify secondarily the interaction of APOA5 with the lipoprotein lipase and result ultimately in increased circulating triglyceride levels.…”
Section: Discussionmentioning
confidence: 99%