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 ?
USF1 y USF2 forman un heterodimero, el cual se une a regiones del promotor (Caja-E) e inicia la transcripcion de distintos genes tales como el gen de la apoAV, apoC-III, ApoA-II, ApoE, lipasa sensible a hormonas, sintasa de acidos grasos, acetilCoA carboxilasa, renina, angiotensinogeno, glucocinasa, receptor de glucagon, insulina, ghrelina, la desaturasa de acidos grasos tipo 3 y la piruvato cinasa hepatica.
They include apoAI, apoAII, apoAIV, apoAV, apoCI, apoCII, apoCIII and apoE as well as several lesser-known apoproteins.
ApoAV decreases plasma triglycerides by inhibiting very low density lipoprotein-triglyceride (VLDL-TG) pro duction and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis.
Postprandial increase of plasma apoAV concentrations in type 2 diabetic patients.
ApoAV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglyceride production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis.
(1) recently reported an association between a distinct combination of variants in the apolipoprotein E (APOE) and APOAV genes and hypertriglyceridemia.
APOAV variants (e.g., T-1131>C and Ser19>Trp) play an important role in modulating plasma TG concentrations in humans (4).
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 this context, the newly identified apo AV gene (APOAV) (10,11), adjacent to the AI-CIII-AIV gene cluster and with a clear impact on TG metabolism in animals (10), becomes a candidate.
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).