DIFFERENTIAL RESPONSES OF INTESTINAL GLUCOSE-TRANSPORTER MESSENGER-RNA TRANSCRIPTS TO LEVELS OF DIETARY SUGARS

Citation
K. Miyamoto et al., DIFFERENTIAL RESPONSES OF INTESTINAL GLUCOSE-TRANSPORTER MESSENGER-RNA TRANSCRIPTS TO LEVELS OF DIETARY SUGARS, Biochemical journal, 295, 1993, pp. 211-215
Citations number
41
Categorie Soggetti
Biology
Journal title
ISSN journal
02646021
Volume
295
Year of publication
1993
Part
1
Pages
211 - 215
Database
ISI
SICI code
0264-6021(1993)295:<211:DROIGM>2.0.ZU;2-B
Abstract
Dietary sugars are known to stimulate intestinal glucose transport act ivity, but the specific signals involved are unknown. The Na+-dependen t glucose co-transporter (SGLT1), the liver-type facilitative glucose transporter (GLUT2) and the intestinal-type facilitative glucose trans porter (GLUT5) are all expressed in rat jejunum [Miyamoto, Hase, Taket ani, Minami, Oka, Nakabou and Hagihira (1991) Biochem. Biophys. Res. C ommun. 181, 1110-1117]. In the present study we have investigated the effects of dietary sugars on these glucose transporter genes. A high-g lucose diet stimulated glucose transport activity and increased the le vels of SGLTI and GLUT2 mRNAs in rat jejunum. 3-O-Methylglucose, D-gal actose, D-fructose, D-mannose and D-xylose can mimic the regulatory ef fect of glucose on the SGLT1 mRNA level in rat jejunum. However, only D-galactose and D-fructose increased the levels of GLUT2 mRNA. The GLU T5 mRNA level was increased significantly only by D-fructose. Our resu lts suggest that the increase in intestinal transport activity in rats caused by dietary glucose is due to an increase in the levels of SGLT 1 and GLUT2 mRNAs. and that these increases in mRNA may be caused by a n enhancement of the transcriptional rate. Furthermore, for expression of the SGLT1 gene, the signal need not be a metabolizable or transpor table substrate whereas, for expression of the GLUT2 gene. metabolism of the substrate in the liver may be necessary for signalling. Only D- fructose is an effective signal for expression of the GLUT5 gene.