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[载脂蛋白基因的营养调控。膳食碳水化合物和脂肪酸的影响]

[Nutritional regulation of apolipoprotein genes. Effect of dietary carbohydrates and fatty acids].

作者信息

Ribeiro A, Mangeney M, Cardot P, Loriette C, Chambaz J, Rayssiguier Y, Bereziat G

机构信息

Equipe de Recherche sur la Biologie Cellulaire et Moléculaire des Médiateurs lipidiques et des lipoprotéines (CNRS URA 1283), CHU Saint-Antoine, Université Pierre et Marie Curie, France.

出版信息

Diabete Metab. 1992;18(1 Pt 2):137-44.

PMID:1563548
Abstract

The effect of nutritional factors on apolipoprotein gene expression by rat liver were studied. Dietary carbohydrates or fatty acids regulate the expression of apo E gene, by altering either gene transcription or mRNA stability. Conversely, apo A1 regulation occurs at a post transcriptional level. In vivo and in vitro experiments gave contradictory results concerning apo B gene expression. The more dramatic changes in plasma lipids and apolipoproteins are obtained under dietary fish oil. Hepatocytes from fish oil-fed rats retain for several days modification in fatty acid metabolism, i.e. a shift in oleic acid channeling towards oxidation at the expense of esterification and a reduced ability to synthesize and secrete triacylglycerol. These modifications are paralleled with a decrease in the synthesis and in the secretion of apo Bs. Hepatocytes from fish oil fed rats secrete degradative forms of apo B which might result from either a sluggish VLDL synthesis and secretion or a more specific effect of n-3 long chain polyunsaturated fatty acid peroxidative products. Hepatocytes from fish oil fed rats exhibit a reduced ability to synthesize cholesterol, associated with a decrease in apo A1 synthesis and secretion without any modification in apo A1 mRNA. In contrast, the hepatocytes exhibit a concomitent decrease in apo E synthesis and secretion and in cellular apo E mRNA levels.

摘要

研究了营养因素对大鼠肝脏载脂蛋白基因表达的影响。膳食碳水化合物或脂肪酸通过改变基因转录或mRNA稳定性来调节载脂蛋白E基因的表达。相反,载脂蛋白A1的调节发生在转录后水平。体内和体外实验关于载脂蛋白B基因表达给出了相互矛盾的结果。在膳食鱼油作用下,血浆脂质和载脂蛋白发生更为显著的变化。鱼油喂养大鼠的肝细胞在脂肪酸代谢方面的改变会持续数天,即油酸流向氧化的通道发生改变,以酯化作用为代价,合成和分泌三酰甘油的能力降低。这些改变与载脂蛋白B的合成和分泌减少同时出现。鱼油喂养大鼠的肝细胞分泌载脂蛋白B的降解形式,这可能是由于极低密度脂蛋白合成和分泌迟缓,或者是n-3长链多不饱和脂肪酸过氧化产物的更特异性作用。鱼油喂养大鼠的肝细胞合成胆固醇的能力降低,并伴有载脂蛋白A1合成和分泌减少,而载脂蛋白A1 mRNA没有任何改变。相反,肝细胞中载脂蛋白E的合成、分泌以及细胞内载脂蛋白E mRNA水平均同时降低。

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