Differential responses of intestinal glucose transporter mRNA transcripts to levels of dietary sugars

• Published in: Biochemical journal 1993-10, Vol.295 (1), p.211-215
• Main Authors: Miyamoto, K, Hase, K, Takagi, T, Fujii, T, Taketani, Y, Minami, H, Oka, T, Nakabou, Y
• Format: Article
• Language: English
• Subjects: Analytical, structural and metabolic biochemistry; Animals; Binding and carrier proteins; Biological and medical sciences; Biological Transport; Cell Nucleus - metabolism; dietary carbohydrate; Dietary Carbohydrates - pharmacology; DNA, Complementary; Fundamental and applied biological sciences. Psychology; Galactose - metabolism; genetic regulation; glucose; Glucose - pharmacology; glucose transporter; Glucose Transporter Type 2; Glucose Transporter Type 5; Hexoses - pharmacology; In Vitro Techniques; Intestine, Small - metabolism; Jejunum - metabolism; Male; messenger RNA; Monosaccharide Transport Proteins - genetics; nutrient transport; Proteins; Rats; Rats, Sprague-Dawley; RNA, Messenger - biosynthesis; sugars; Transcription, Genetic
• ISSN: 0264-6021; 1470-8728
• DOI: 10.1042/bj2950211

Dietary sugars are known to stimulate intestinal glucose transport activity, but the specific signals involved are unknown. The Na(+)- dependent glucose co-transporter (SGLT1), the liver-type facilitative glucose transporter (GLUT2) and the intestinal-type facilitative glucose transporter (GLUT5) are all expressed in rat jejunum [Miyamoto, Hase, Taketani, Minami, Oka, Nakabou and Hagihira (1991) Biochem. Biophys. Res. Commun. 181, 1110-1117] In the present study we have investigated the effects of dietary sugars on these glucose transporter genes. A high-glucose diet stimulated glucose transport activity and increased the levels of SGLT1 and GLUT2 mRNAs in rat jejunum. 3-O- Methylglucose, D-galactose, D-fructose, D-mannose and D-xylose can mimic the regulatory effect of glucose on the SGLT1 mRNA level in rat jejunum. However, only D-galactose and D-fructose increased the levels of GLUT2 mRNA. The GLUT5 mRNA level was increased significantly only by D-fructose. Our results suggest that the increase in intestinal transport activity in rats caused by dietary glucose is due to an increase in the levels of SGLT1 and GLUT2 mRNAs, and that these increases in mRNA may be caused by an enhancement of the transcriptional rate. Furthermore, for expression of the SGLT1 gene, the signal need not be a metabolizable or transportable 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.