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 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.
Jiang
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Graduate School of the Biomedical Sciences, Newark, New Jersey 07103-2714, USA.
Ferraris
R P
RP
D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005632:Fructose / Q000493:pharmacokinetics; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D005947:Glucose / Q000493:pharmacokinetics; D051296:Glucose Transporter Type 5; D007408:Intestinal Absorption / Q000502:physiology*; D007413:Intestinal Mucosa / Q000254:growth & development / Q000378:metabolism; D007421:Intestine, Small / Q000254:growth & development* / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000235:genetics* / Q000378:metabolism; D010477:Perfusion; D011247:Pregnancy; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D051269:Sodium-Glucose Transporter 1; D015996:Survival Rate; D014158:Transcription, Genetic / Q000187:drug effects / Q000502:physiology
D051296:Glucose Transporter Type 5; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D011500:Protein Synthesis Inhibitors; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; C495676:Slc5a1 protein, rat; D051269:Sodium-Glucose Transporter 1; D003609:Dactinomycin; D005632:Fructose; D003513:Cycloheximide; D012964:Sodium; D005947:Glucose