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首页> 外文期刊>American Journal of Physiology >Uptake and metabolism of structured triglyceride by Caco-2 cells: reversal of essential fatty acid deficiency.
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Uptake and metabolism of structured triglyceride by Caco-2 cells: reversal of essential fatty acid deficiency.

机译:Caco-2细胞摄取和代谢结构化甘油三酸酯:逆转必需脂肪酸缺乏症。

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摘要

Structured lipids have been proposed as efficient vehicles for the supplementation of essential fatty acids (EFA) to patients with malabsorption. We investigated how a novel structured triglyceride (STG), containing purely octanoic acid in the sn-1/sn-3 and [14C]linoleic acid in the sn-2 positions, was incorporated into different lipid classes in Caco-2 cells. We also evaluated the contribution of gastric lipase in the uptake and metabolism of [14C]linoleic acid from the STG. We furthermore determined the potential of the STG to correct EFA deficiency induced in Caco-2 cells. The absorption of STG by Caco-2 cells was significantly greater compared with that of triolein. The addition of human gastric lipase significantly enhanced cellular uptake of the labeled substrate, reflecting the stereoselectivity of gastric lipase to hydrolyze medium chain FA. Analysis of the intracellular lipids synthesized revealed a predominance of phospholipids-monoglycerides. Most of the radioactivity in the lipoproteins isolated from Caco-2 cells was recovered in TG-rich lipoproteins (45%) and to a lesser extent in the high-density lipoprotein (36%) and low-density lipoprotein (17%) fractions. The administration of STG to Caco-2 cells rendered EFA deficient produced a marked increase of the cellular level of linoleic and arachidonic acids. This resulted in a lower ratio of 20:3(n-9) to 20:4(n-6), reflecting the correction of EFA deficiency in Caco-2 cells. Our data demonstrate that STG, in the presence of gastric lipase, have beneficial effects on lipid incorporation, lipoprotein production, and EFA status, utilizing Caco-2 cells as a model of EFA deficiency.
机译:已经提出结构脂质是向吸收不良患者补充必需脂肪酸(EFA)的有效载体。我们研究了如何将新型的结构化甘油三酸酯(STG)包含在sn-1 / sn-3中的纯辛酸和sn-2位置的[14C]亚油酸,掺入Caco-2细胞的不同脂质类别中。我们还评估了胃脂肪酶在STG吸收和代谢[14C]亚油酸中的作用。我们还确定了STG纠正Caco-2细胞中诱导的EFA缺乏的潜力。与三油精相比,Caco-2细胞对STG的吸收明显更大。人胃脂肪酶的添加显着增强了标记底物的细胞摄取,反映了胃脂肪酶水解中链FA的立体选择性。对合成的细胞内脂质的分析表明,磷脂-甘油单酸酯占优势。从Caco-2细胞分离出的脂蛋白中的大多数放射性都在富含TG的脂蛋白(45%)中回收,而在高密度脂蛋白(36%)和低密度脂蛋白(17%)组分中回收的程度较小。将STG施用至Caco-2细胞使EFA缺乏,可导致亚油酸和花生四烯酸的细胞水平显着增加。这导致20:3(n-9)与20:4(n-6)的比率降低,反映了Caco-2细胞中EFA缺乏症的纠正。我们的数据表明,在胃脂肪酶存在的情况下,STG利用Caco-2细胞作为EFA缺乏症的模型,对脂质掺入,脂蛋白生成和EFA状况具有有益作用。

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