APOA5

(redirected from APOAV)

APOA5

A gene on chromosome 11q23 that encodes apolipoprotein A-V, a minor apolipoprotein mainly associated with high-density lipoprotein (HDL), less so with VLDL and chylomicrons. It is an important determinant of plasma triglyceride (TG) levels, both stimulating TG hydrolysis by apo-CII lipoprotein lipase and inhibiting VLDL-TG production.
References in periodicals archive ?
1) recently reported an association between a distinct combination of variants in the apolipoprotein E (APOE) and APOAV genes and hypertriglyceridemia.
Using a previously described method, we have analyzed (by PCR and restriction analysis) APOE and APOAV variants (T-1131>C, Ser19> Trp, and Va1153>Met) (6,11) in 2559 unrelated Caucasians.
1), we found no significant interaction between the APOAV Trp19 variant, APOE2, and hypertriglyceridemia: of 111 HTG patients, 4 were carriers of the APOE22 genotype and 1 of these had the APOAV Trp19 allele.
In the population sample of 2559 individuals, we detected 20 APOE22 homozygotes, and 4 of them also had the APOAV Trp19 allele.
Finally, of 8 APOE22 homozygotes with type III hyperlipidemia, only 3 were carriers of the APOAV Trp19 allele.
The other APOAV variants (T-1131C and Va1153Met) exhibit no interaction with APOE in the genetic determination of different forms of hypertriglyceridemia (details not shown).
Associations were analyzed between the APOAV gene and TG metabolism in a population-based Spanish control group (12) (ESP controls; n = 408), a normolipidemic control group from The Netherlands (13) (NL controls; n = 89), and 16 FCHL families (9) (n = 103) with 42 hyperlipidemic and 61 normolipidemic first-degree relatives.
Among the FCHL families, there was a significant association between the APOAV marker and TG-related variables, but when adjusted for age, gender, body mass index, or diet, these associations were not significant in the control ESP group or the normolipidemic NL group (Table 1).
Altogether these data suggest that in FCHL families, carriers of at least one rare APOAV allele will have a 3.
10) reported negative linkage disequilibrium between markers of the AI-CIII-AIV gene cluster and APOAV, indicating an independent effect of APOAV on plasma TG concentrations.
11) speculated that apo AV might antagonize lipid uptake by the liver, which could explain the association of APOAV with plasma TGs.
However, the fact that APOAV is associated with increased VLDL-apo B but not with total or LDL-apo B suggests that apo AV might be involved in the delay of peripheral TG hydrolysis.