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载脂蛋白M(apoM)是lipocalin家族成员,其表达具有组织特异性。血小板活化因子(PAF)能增加apoM以及apoM mRNA在Hepg2细胞中的表达,而PAF受体拮抗剂(lexipafant)能抑制apoM的表达。apoM血清水平的高低与肝细胞核因子(HNF-1a)浓度有关,胰岛素在体内也调节apoM的生成。瘦素(Leptin)特异性调节apoM的分泌。apoM大部分存在于高密度脂蛋白(HDL)中,影响HDL的代谢并具有抗动脉粥样硬化作用。通过对apoA-I缺陷小鼠研究发现:正常小鼠体内apoM与apoA-I代谢有关。在低密度脂蛋白(LDL)与HDL中apoM存在5个亚型。在汉族人群中apoM基因的核苷酸778C等位基因以及855C均能增加患冠状动脉粥样硬化的危险性。apoM似乎与2型糖尿病患者的动脉粥样硬化的因子相关。
Apolipoprotein M (apoM) is a member of the lipocalin family whose expression is tissue specific. Platelet-activating factor (PAF) increases apoM and apoM mRNA expression in Hepg2 cells, whereas PAF receptor antagonist (lexipafant) inhibits apoM expression. The level of apoM serum is related to the concentration of hepatocyte nuclear factor (HNF-1a), which also regulates apoM production in vivo. Leptin specifically regulates the secretion of apoM. ApoM is mostly present in high-density lipoproteins (HDLs), affecting HDL metabolism and having anti-atherogenic effects. ApoA-I deficient mice through the study found: apoM in normal mice and apoA-I metabolism. There are 5 subtypes of apoM in low-density lipoprotein (LDL) and HDL. In the Han population apoM gene nucleotide 778C allele and 855C can increase the risk of coronary atherosclerosis. ApoM appears to be associated with atherosclerosis in patients with type 2 diabetes.