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Studies on the gene expression and physiological roles of cellular retinol-binding protein, type II in small intestine

小肠细胞视黄醇结合蛋白 II 型的基因表达和生理作用研究

基本信息

批准号：
09670074
负责人：
TAKASE Sachiko
金额：
$ 2.37万
依托单位：
University of Shizuoka
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

项目摘要

1) We investigated the mechanism whereby dietary fatty acids modulate the gene expression of cellular retinol-binding protein, type II (CRBP(II)) in the small intestine. The rats fed the high-fat diet showed a parallel increase in the transcription of CRBP(II) gene and the level of PPAROalpha mRNA, which was accompanied by an increase in the amount of nuclear proteins (including PPAR-RXR heterodimer) binding to the nuclear receptor-response elements located in the promoter of CRBP(II) gene. The mRNA level of a PPAR subtype (PPARdelta) was reduced in the small intestine by dietary fat. Inhibitors of enzymes involved in arachidonic acid metabolism did not influence the dietary fat- induced increase in the CRBP(II) gene expression. Transfection experiments revealed that CRBP(II) gene expression is induced by fatty acids through activation of PPAR-RXR heterodimer.2) Gene expressions of CRBP(II) and L-type fatty acid-binding protein (L-FABP) exhibited a coordinated diurnal variation in rat small intestine. Both CRBP(II) and L-FABP mRNA levels were elevated at feeding periods, attributable to the dietary fat-induced increase in the transcription of these two genes.3) Effects of starvation on the mRNA levels of CRBP(II), L-FABP and I-FABP were investigated in rat jejunum. The mRNA levels of these three genes decreased in parallel on day 1, but increased above the non- starved control level on day 3 of starvation. These variations corresponded with the changes in the amount of triacylglycerols in jejunal tissue, and may have reflected the amount of fatty acids coming into the enterocytes.4) Feeding excessive beta-carotene to rats enhanced the beta-carotene cleavage enzyme activity in the jejunum, while it caused a decrease in retinal reductase activity in the jejunum. This result suggests that the conversion of retinal to retinol is down-regulated by excesive intake of dietary beta-carotene.

1)我们研究了膳食脂肪酸调节小肠中细胞视黄醇结合蛋白II型（CRBP（II））基因表达的机制。高脂饮食大鼠显示CRBP（II）基因转录和PPARO α mRNA水平平行增加，这伴随着与位于CRBP（II）基因启动子的核受体反应元件结合的核蛋白（包括PPAR-RXR异源二聚体）的量增加。小肠中的PPAR亚型（PPARdelta）的mRNA水平因膳食脂肪而降低。花生四烯酸代谢相关酶的抑制剂不影响膳食脂肪诱导的CRBP（II）基因表达的增加。转染实验表明，脂肪酸通过激活PPAR-RXR异源二聚体诱导CRBP（II）基因表达。2）大鼠小肠CRBP（II）和L型脂肪酸结合蛋白（L-FABP）基因表达呈现协调的昼夜变化。3）研究了饥饿对大鼠空肠CRBP（II）、L-FABP和I-FABP mRNA水平的影响。这三个基因的mRNA水平在饥饿第1天平行下降，但在饥饿第3天增加到高于非饥饿对照水平。这些变化与空肠组织中三酰甘油含量的变化相对应，并可能反映了进入肠细胞的脂肪酸含量。4）喂饲过量β-胡萝卜素可增强空肠中β-胡萝卜素裂解酶的活性，同时导致空肠中视黄醇还原酶活性降低。这一结果表明，大量摄入膳食β-胡萝卜素会下调视黄醇向视黄醇的转化。