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大鼠肠黏膜中GLUT5基因表达的调控:区域分布、昼夜节律、围产期发育及糖尿病的影响。

Regulation of GLUT5 gene expression in rat intestinal mucosa: regional distribution, circadian rhythm, perinatal development and effect of diabetes.

作者信息

Castelló A, Gumá A, Sevilla L, Furriols M, Testar X, Palacín M, Zorzano A

机构信息

Departament de Bioquímica i Fisiologia, Facultat de Biologia, Universitat de Barcelona, Spain.

出版信息

Biochem J. 1995 Jul 1;309 ( Pt 1)(Pt 1):271-7. doi: 10.1042/bj3090271.

DOI:10.1042/bj3090271
PMID:7619068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1135830/
Abstract
  1. GLUT5 gene expression was studied in small intestine under a variety of conditions characterized by altered intestinal absorption of monosaccharides. 2. RNA-blotting studies showed that GLUT5 mRNA was abundantly expressed in rat and rabbit intestine and kidney, but it was not detected in heart or brown adipose tissue. GLUT5 mRNA levels were higher in the upper segments of the small intestine (duodenum and proximal jejunum) than in the lower segments (distal jejunum and ileum). 3. The intestinal expression of GLUT5 mRNA in rat proximal jejunum showed circadian rhythm. A 12-fold increase in GLUT5 mRNA levels was detected at the end of the light cycle and at the beginning of the dark cycle when compared with the early light period. In keeping with this, GLUT5 protein content in brush-border membranes was also increased at the beginning of the dark cycle compared with that in the light period. 4. In streptozotocin-induced diabetes an 80% increase in GLUT5 mRNA levels in mucosa from the proximal jejunum was detected under conditions in which enhanced intestinal absorption of monosaccharides has been reported. 5. The intestinal expression of GLUT5 mRNA showed regulation during perinatal development. Levels of GLUT5 mRNA were low during fetal life, increased progressively during the postnatal period and reached levels comparable with the adult state after weaning. Weaning on to a high-fat diet partially prevented the induction of GLUT5 gene expression. 6. Our results indicate that GLUT5 gene expression is tightly regulated in small intestine. Regulation involves maximal expression in the upper part of the small intestine, circadian rhythm, developmental regulation dependent on the fat and carbohydrate content in the diet at weaning and enhanced expression in streptozotocin-induced diabetes. Furthermore, changes observed in intestinal GLUT5 expression correlate with reported alterations in intestinal absorption of fructose. This suggests a regulatory role for GLUT5 in fructose uptake by absorptive enterocytes.
摘要
  1. 在多种以单糖肠道吸收改变为特征的条件下,研究了小肠中葡萄糖转运蛋白5(GLUT5)基因的表达。2. RNA印迹研究表明,GLUT5 mRNA在大鼠和兔的小肠及肾脏中大量表达,但在心脏或棕色脂肪组织中未检测到。小肠上段(十二指肠和空肠近端)的GLUT5 mRNA水平高于下段(空肠远端和回肠)。3. 大鼠空肠近端GLUT5 mRNA的肠道表达呈现昼夜节律。与光照早期相比,在光照周期结束时和黑暗周期开始时,GLUT5 mRNA水平增加了12倍。与此一致的是,与光照期相比,刷状缘膜中的GLUT5蛋白含量在黑暗周期开始时也增加了。4. 在链脲佐菌素诱导的糖尿病中,在报道有单糖肠道吸收增强的条件下,检测到空肠近端黏膜中GLUT5 mRNA水平增加了80%。5. GLUT5 mRNA的肠道表达在围产期发育过程中受到调节。胎儿期GLUT5 mRNA水平较低,出生后逐渐升高,断奶后达到与成年状态相当的水平。断奶后采用高脂饮食可部分阻止GLUT5基因表达的诱导。6. 我们的结果表明,GLUT5基因表达在小肠中受到严格调控。调控包括在小肠上部的最大表达、昼夜节律、断奶时依赖饮食中脂肪和碳水化合物含量的发育调控以及链脲佐菌素诱导的糖尿病中的表达增强。此外,观察到的肠道GLUT5表达变化与报道的果糖肠道吸收改变相关。这表明GLUT5在吸收性肠细胞摄取果糖中起调节作用。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/0ae52805a9fe/biochemj00060-0264-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/821b75be0b82/biochemj00060-0261-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/2f2af6fa87ff/biochemj00060-0262-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/5e0e68c230cb/biochemj00060-0262-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/818d73023a27/biochemj00060-0262-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/25a5091f933f/biochemj00060-0263-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/f925ef8adbd3/biochemj00060-0263-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/f939dcc3c96b/biochemj00060-0264-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/0ae52805a9fe/biochemj00060-0264-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/821b75be0b82/biochemj00060-0261-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/2f2af6fa87ff/biochemj00060-0262-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/5e0e68c230cb/biochemj00060-0262-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/818d73023a27/biochemj00060-0262-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/25a5091f933f/biochemj00060-0263-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/f925ef8adbd3/biochemj00060-0263-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/f939dcc3c96b/biochemj00060-0264-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0ae/1135830/0ae52805a9fe/biochemj00060-0264-b.jpg

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