APOA4

APOA4

A gene on chromosome 11q23 that encodes apolipoprotein A-IV, which is a major component of high-density lipoprotein (HDL) and chylomicrons. It plays a role in chylomicrons and VLDL secretion and catabolism, and is required for efficient activation of lipoprotein lipase by ApoC-II. It is a potent activator of lecithin-cholesterol acyltransferase (LCAT).
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Los biomarcadores candidatos para identificar el fenotipo MHO son los niveles de expresion de las proteinas glicoproteina [alfa]-2HS (AHSG), la RBP4 y la APOA4 (66).
MARS/ mR- Veinte proteinas se (66) PLC-MS/M expresaron diferencialmente entre mujeres metabolicamente sanas y con alteraciones metabolicas; algunas proteinas diferenciales fueron las subunidades de hemoglobina (HBA1, P5), la proteina relacionada con haptoglobina (HPR) y las apolipoproteinas APOB100, APOA4, RBP4 y CRP.
Four proteins, A2M, GC, C4, and APOA4, were identified in five pathways which may be related with hypocalcemia, including the "Endocrine and other factor-regulated Ca reabsorption" (ID: 04961), "Mineral absorption" (ID: 04978), "Complement and coagulation cascades" (ID: 04611), "Fat digestion and absorption" (ID: 04975) and "Vitamin digestion and absorption" (ID: 04977) (Table 3).
3] with APOA4 enter the chylomicron, then the chylomicron is exocytosed to the extracellular space and finally enters the blood via lymph transfer.
The result of this study showed that APOA4 was down-regulated in the CH group, as compared with the C and SH groups, while there was no significant different between the C and SH groups.
On the other hand, notes Ordovas, "people with a specific mutation of the APOA4 gene have less than half as much improvement in blood lipids from the cholesterol-lowering diet as those with no mutation.
Three years ago, Ordovas enlisted a group of researchers at the University of Cordoba Medical School in his native Spain to study a gene-diet interaction with still another of the seven known mutations of the APOA4 gene.
So the Spanish researchers, under Ordovas' guidance, looked for a gene-gene interaction between these APOA1 and APOA4 mutations.
Although all these apolipoprotein genes have been found to be related to obesity in at least one epidemiological study (20), only APOA4 has been subscribed in regulation of food intake, acting as a satiety signal (21).
39) were the first to report that APOA4 is a satiety factor secreted by the intestine after fat absorption and that this function of APOA4 is not shared by gut APOA1.
APOE did so singly, however, and the combination of SNPs in the genes for UCP2, APOA4, and LPL with APOE improved prediction further.
The CHD-risk mechanism of action of the functional SNPs is thus attributable to modulation of the anti- or proatherogenic actions of the cognate proteins, with the APOE effect probably related to the associated atherogenicity of plasma lipoproteins (28, 35), the influence of UCP2 on oxidative stress (39), the reverse cholesterol metabolism and lipid oxidation effects of APOA4 (40), the influence of LPL (34) and PECAM1 (41) on monocyte adhesion and entry into the developing plaque, and the modulation by IL6 of IL-6 plasma and tissue concentrations and thus damage to endothelial or other vascular wall cells (reviewed in Ref.