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

Fructose transporter (GLUT-5) expression is low in mid-weaning rat small in testine, increases normally after weaning is completed, and can be precocio usly induced by premature consumption of a high-fructose (HF) diet. In this study, an in vivo perfusion model was used to determine the mechanisms reg ulating 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 expr ession. Intraperitoneal injection of actinomycin D before intestinal perfus ion 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 S GLT-1 mRNA abundance. Cycloheximide blocked the HF-induced increase in fruc tose uptake rate but not the increase in GLUT-5 mRNA abundance and had no e ffect on glucose uptake rate and SGLT-1 mRNA abundance. In neonatal rats, t he substrate-induced reprogramming of intestinal fructose transport is like ly to involve transcription and translation of the GLUT-5 gene.