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[肠道载脂蛋白代谢]

[Intestinal apolipoprotein metabolism].

作者信息

Steinmetz A

机构信息

Abteilung Endokrinologie und Stoffwechsel, Philipps-Universität Marburg/Lahn.

出版信息

Klin Wochenschr. 1990;68 Suppl 22:12-8.

PMID:2087069
Abstract

Intestinal apolipoproteins play a major role in lipoprotein metabolism. Apolipoproteins (Apo) AI, AIV and B48 are synthesized with chylomicrons in the mucosa and secreted into intestinal lymph. Apo B48 and B100 are coded for by the same gene on chromosome 2 and are identical in their aminoterminus. While apo B100 mRNA can be translated to the 4536 amino acid protein, the apo B48 mRNA is edited to contain a stopcodon at amino acid 2152. Apo B48 seems to be important for the secretion of chylomicrons and stays with chylomicrons during their lipolysis in plasma. Hydrolysis only takes place after the particle has acquired apo CII, the obligate cofactor for the enzyme lipoprotein lipase. The ligand for final irreversible uptake into the liver, mediated by a putative chylomicron-remnant receptor, seems to be apo E which only associates during lipolysis in plasma. Although apo E is not synthesized to a significant extent in the gut it was reported to influence intestinal cholesterol absorption: carriers of the genetic apo E2 isoform seem to absorb cholesterol to a lesser extent than those with apo E4 as compared to apo E3. Despite the almost exclusive synthesis of apo AIV and the significant extent of apo AI synthesis in the human gut these two apoproteins do not seem to have a chylomicron specific function. They seem to be more involved in the "reversed cholesterol transport", believed to be antiatherogenic. After entering the plasma compartment apo AI and AIV leave the chylomicrons during lipolysis as "surface remnants" to become high density- (HDL)-and apo AIV containing lipoproteins.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肠道载脂蛋白在脂蛋白代谢中起主要作用。载脂蛋白(Apo)AI、AIV和B48在黏膜中与乳糜微粒一起合成,并分泌到肠淋巴中。Apo B48和B100由2号染色体上的同一基因编码,其氨基末端相同。虽然apo B100 mRNA可被翻译成含4536个氨基酸的蛋白质,但apo B48 mRNA经编辑后在第2152个氨基酸处含有一个终止密码子。Apo B48似乎对乳糜微粒的分泌很重要,并在其于血浆中进行脂解时与乳糜微粒保持在一起。只有在微粒获得酶脂蛋白脂酶的必需辅助因子apo CII后才会发生水解。由假定的乳糜微粒残粒受体介导的最终不可逆摄取进入肝脏的配体似乎是apo E,它仅在血浆脂解过程中缔合。尽管apo E在肠道中合成量很少,但据报道它会影响肠道胆固醇吸收:与apo E3相比,遗传apo E2异构体的携带者似乎比apo E4携带者吸收胆固醇的程度更低。尽管在人类肠道中几乎仅合成apo AIV且apo AI合成量很大,但这两种载脂蛋白似乎不具有乳糜微粒特异性功能。它们似乎更多地参与“逆向胆固醇转运”,这被认为具有抗动脉粥样硬化作用。进入血浆区室后,apo AI和AIV在脂解过程中作为“表面残粒”离开乳糜微粒,成为含高密度脂蛋白(HDL)和apo AIV的脂蛋白。(摘要截短于250词)

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