Developmental reprogramming of rat GLUT-5 requires de novo mRNA and protein synthesis

• Published in: American journal of physiology: Gastrointestinal and liver physiology 2001-01, Vol.280 (1), p.G113-G120
• Main Authors: Jiang, L, Ferraris, R P
• Format: Article
• Language: English
• Subjects: Animals; Cycloheximide - pharmacology; Dactinomycin - pharmacology; Dose-Response Relationship, Drug; Female; Fructose - pharmacokinetics; Gene Expression Regulation, Developmental - physiology; Glucose - pharmacokinetics; Glucose Transporter Type 5; Intestinal Absorption - physiology; Intestinal Mucosa - growth & development; Intestinal Mucosa - metabolism; Intestine, Small - growth & development; Intestine, Small - metabolism; Male; Membrane Glycoproteins - genetics; Membrane Glycoproteins - metabolism; Monosaccharide Transport Proteins - genetics; Monosaccharide Transport Proteins - metabolism; Perfusion; Pregnancy; Protein Synthesis Inhibitors - pharmacology; Proto-Oncogene Proteins c-fos - genetics; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; Sodium - metabolism; Sodium-Glucose Transporter 1; Survival Rate; Transcription, Genetic - drug effects; Transcription, Genetic - physiology
• ISSN: 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.2001.280.1.g113

Fructose transporter (GLUT-5) expression is low in mid-weaning rat small intestine, increases normally after weaning is completed, and can be precociously induced by premature consumption of a high-fructose (HF) diet. In this study, an in vivo perfusion model was used to determine the mechanisms regulating this substrate-induced reprogramming of GLUT-5 development. HF (100 mM) but not high-glucose (HG) perfusion increased GLUT-5 activity and mRNA abundance. In contrast, HF and HG perfusion had no effect on Na(+)-dependent glucose transporter (SGLT-1) expression but increased c-fos and c-jun expression. Intraperitoneal injection of actinomycin D before intestinal perfusion blocked the HF-induced increase in fructose uptake rate and GLUT-5 mRNA abundance. Actinomycin D also prevented the perfusion-induced increase in c-fos and c-jun mRNA abundance but did not affect glucose uptake rate and SGLT-1 mRNA abundance. Cycloheximide blocked the HF-induced increase in fructose uptake rate but not the increase in GLUT-5 mRNA abundance and had no effect on glucose uptake rate and SGLT-1 mRNA abundance. In neonatal rats, the substrate-induced reprogramming of intestinal fructose transport is likely to involve transcription and translation of the GLUT-5 gene.