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猪的必需脂肪酸缺乏症:对类花生酸基础水平及小肠体外合成的影响。

Essential fatty acid deficiency in the pig: effects on eicosanoid basal levels and in vitro synthesis by the small intestine.

作者信息

Clément G, Christon R, Créminon C, Frobert Y, Pradelles P, Wal J M

机构信息

Laboratoire Associé INRA-CEA, DRIPP, SPI, CE Saclay, Gif/Yvette, France.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1994 Mar;50(3):147-54. doi: 10.1016/0952-3278(94)90098-1.

Abstract

The influence of nutritional essential fatty acid (EFA) deficiency on arachidonate metabolism by porcine small intestine has been studied. Great care was exercised in the manipulation of the jejunal wall to avoid artefactual metabolism of arachidonate. Thus, jejunal wall was frozen in liquid nitrogen after organ removal and washing, and subsequently lyophilized. This lyophilized tissue was used as starting material for all experiments, including organic solvent extractions (for basal level determinations) and reconstitution in aqueous buffer (for neosynthesis experiments). Feeding pigs with a low linoleate diet for 12 weeks resulted in a 36% diminution in the % of arachidonate in jejunal phospholipids. Basal levels of 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha), thromboxane B2 (TXB2), PGF2 alpha, PGE2, PGD2 and leukotriene B4 (LTB4) were not altered in the EFA-deficient state. However, we observed a significant lowering of the synthesis of each of these eicosanoids (except LTB4) by the EFA-deficient jejunum during brief (15s) in vitro neosynthesis experiments. The origin of arachidonate as a substrate of PG endoperoxide synthase, also named PGH synthase or cyclooxygenase (Cox) in these neosynthesis experiments is probably a non-esterified fatty acid pool since, (1) neosynthesis was not inhibited by the phospholipase A2 (PLA2) inhibitor parabromophenacylbromide, and (2) substantial amounts of arachidonic acid were found in the jejunum, frozen or lyophilized. Cox activity of the lyophilized jejunum and Cox content of liver and intestine microsomes were not modified in the EFA-deficient state.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了营养必需脂肪酸(EFA)缺乏对猪小肠花生四烯酸代谢的影响。在操作空肠壁时格外小心,以避免花生四烯酸的人为代谢。因此,在器官切除和冲洗后,将空肠壁在液氮中冷冻,随后冻干。这种冻干组织用作所有实验的起始材料,包括有机溶剂萃取(用于基础水平测定)和在水性缓冲液中重构(用于新合成实验)。用低亚油酸饮食喂养猪12周导致空肠磷脂中花生四烯酸百分比降低36%。在EFA缺乏状态下,6-酮前列腺素F1α(6-酮PGF1α)、血栓素B2(TXB2)、PGF2α、PGE2、PGD2和白三烯B4(LTB4)的基础水平未改变。然而,在短暂(15秒)的体外新合成实验中,我们观察到EFA缺乏的空肠合成这些类二十烷酸(LTB4除外)的能力显著降低。在这些新合成实验中,作为PG内过氧化物合酶底物的花生四烯酸的来源可能是一个非酯化脂肪酸池,因为:(1)新合成不受磷脂酶A2(PLA2)抑制剂对溴苯甲酰溴的抑制,(2)在冷冻或冻干的空肠中发现了大量花生四烯酸。在EFA缺乏状态下,冻干空肠的Cox活性以及肝脏和小肠微粒体的Cox含量未改变。(摘要截断于250字)

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