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膳食脂肪酸可能是细胞视黄醇结合蛋白II基因表达的关键决定因素。

Dietary fatty acids are possible key determinants of cellular retinol-binding protein II gene expression.

作者信息

Takase S, Tanaka K, Suruga K, Kitagawa M, Igarashi M, Goda T

机构信息

Department of Nutrition, School of Food and Nutritional Sciences, University of Shizuoka, Japan.

出版信息

Am J Physiol. 1998 Apr;274(4):G626-32. doi: 10.1152/ajpgi.1998.274.4.G626.

DOI:10.1152/ajpgi.1998.274.4.G626
PMID:9575843
Abstract

We previously found that dietary unsaturated fatty acids increase cellular retinol-binding protein type II (CRBP II) mRNA and its protein levels in rat jejunum. To obtain insight into mechanisms for its gene induction, we investigated the effect of depletion of dietary fat on CRBP II mRNA levels and we further examined whether dietary retinol is necessary for dietary fat-induced CRBP II gene expression. Feeding the fat-free diet, which contained a sufficient amount of vitamin A, repressed CRBP II mRNA accumulation by 50% within 1 day, and this low level was sustained over the next 9 days. Parallel to the decreased CRBP II mRNA level, the peroxisomal proliferator-activated receptor-alpha (PPAR-alpha) mRNA level in rat jejunum was decreased by long-term (7 days) feeding of an isocaloric low-fat diet compared with the control. Oral administration of corn oil in the animals fed vitamin A-free diet elicited approximately threefold accumulation of CRBP II mRNA within 6 h. However, the administration of 9-cis-retinoic acid brought about no accumulation of CRBP II mRNA. Even when rats were vitamin A-deficient, oral administration of corn oil, but not 9-cis-retinoic acid, caused an increase in jejunal CRBP II mRNA level. These results suggest that CRBP II gene expression in rat jejunum may be regulated predominantly by dietary fatty acids but little by dietary retinoids.

摘要

我们先前发现,膳食不饱和脂肪酸可增加大鼠空肠中细胞视黄醇结合蛋白II(CRBP II)的mRNA及其蛋白水平。为深入了解其基因诱导机制,我们研究了膳食脂肪缺乏对CRBP II mRNA水平的影响,并进一步检测膳食视黄醇对于膳食脂肪诱导的CRBP II基因表达是否必要。喂食含足量维生素A的无脂饮食,1天内CRBP II mRNA积累量就降低了50%,且在接下来的9天内维持在低水平。与CRBP II mRNA水平降低同时,与对照组相比,长期(7天)喂食等热量低脂饮食可使大鼠空肠中过氧化物酶体增殖物激活受体α(PPAR-α)的mRNA水平降低。给喂食无维生素A饮食的动物口服玉米油,6小时内CRBP II mRNA积累量增加约三倍。然而,给予9-顺式视黄酸并未使CRBP II mRNA积累。即使大鼠缺乏维生素A,口服玉米油而非9-顺式视黄酸也会使空肠CRBP II mRNA水平升高。这些结果表明,大鼠空肠中CRBP II基因表达可能主要受膳食脂肪酸调控,而受膳食类视黄醇的调控较少。

相似文献

1
Dietary fatty acids are possible key determinants of cellular retinol-binding protein II gene expression.膳食脂肪酸可能是细胞视黄醇结合蛋白II基因表达的关键决定因素。
Am J Physiol. 1998 Apr;274(4):G626-32. doi: 10.1152/ajpgi.1998.274.4.G626.
2
Unsaturated fatty acids regulate gene expression of cellular retinol-binding protein, type II in rat jejunum.不饱和脂肪酸调节大鼠空肠中II型细胞视黄醇结合蛋白的基因表达。
J Nutr. 1995 Aug;125(8):2039-44. doi: 10.1093/jn/125.8.2039.
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Dietary fat regulates cellular retinol-binding protein II gene expression in rat jejunum.
Biochim Biophys Acta. 1994 May 25;1200(1):34-40. doi: 10.1016/0304-4165(94)90024-8.
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Regulation of vitamin A metabolism-related gene expression.维生素A代谢相关基因表达的调控
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Peroxisome proliferator enhances gene expression of cellular retinol-binding protein, type II in Caco-2 cells.过氧化物酶体增殖剂增强Caco-2细胞中II型细胞视黄醇结合蛋白的基因表达。
Life Sci. 1998;62(10):861-71. doi: 10.1016/s0024-3205(98)00003-4.
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Opposing effects of retinoic acid and dexamethasone on cellular retinol-binding protein ribonucleic acid levels in the rat.
Endocrinology. 1991 Aug;129(2):705-9. doi: 10.1210/endo-129-2-705.
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Diet-related variation in cellular retinol-binding protein type II gene expression in rat jejunum.大鼠空肠中细胞视黄醇结合蛋白II型基因表达的饮食相关变化。
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Transcriptional regulation of cellular retinol-binding protein, type II gene expression in small intestine by dietary fat.膳食脂肪对小肠中II型细胞视黄醇结合蛋白基因表达的转录调控
Arch Biochem Biophys. 1999 Feb 1;362(1):159-66. doi: 10.1006/abbi.1998.1018.
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Gene expression of cellular retinol-binding protein I (CRBP I) is affected by dietary proteins in the rat liver.大鼠肝脏中细胞视黄醇结合蛋白I(CRBP I)的基因表达受膳食蛋白质的影响。
J Nutr Sci Vitaminol (Tokyo). 1993 Dec;39(6):545-54. doi: 10.3177/jnsv.39.545.
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Retinoic acid rapidly induces lung cellular retinol-binding protein mRNA levels in retinol deficient rats.维甲酸能迅速诱导维生素A缺乏大鼠肺细胞视黄醇结合蛋白的mRNA水平。
Biochem Biophys Res Commun. 1988 Oct 31;156(2):712-6. doi: 10.1016/s0006-291x(88)80901-x.

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