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

Am J Physiol Gastrointest Liver Physiol. 2001 Jan;280(1):G113-20. doi: 10.1152/ajpgi.2001.280.1.G113.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 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
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Sodium / metabolism
  • Sodium-Glucose Transporter 1
  • Survival Rate
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / physiology

Substances

  • Glucose Transporter Type 5
  • Membrane Glycoproteins
  • Monosaccharide Transport Proteins
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Proteins c-fos
  • RNA, Messenger
  • Slc5a1 protein, rat
  • Sodium-Glucose Transporter 1
  • Dactinomycin
  • Fructose
  • Cycloheximide
  • Sodium
  • Glucose