The locally acting glucocorticosteroid budesonide enhances intestinal sugar uptake following intestinal resection in rats.
OBJECTIVE
Locally and systemically acting corticosteroids alter the morphology and transport function of the intestine. This study was undertaken to assess the effect of budesonide, prednisone, and dexamethasone on sugar uptake.


METHODS
Adult male Sprague Dawley rats underwent transection or resection of 50% of the middle portion of the small intestine, and in vitro uptake of sugars was measured.


RESULTS
The 50% enterectomy did not alter jejunal or ileal uptake of glucose or fructose. Prednisone had no effect on the uptake of glucose or fructose in resected animals. In contrast, in resected rats budesonide increased by over 120% the value of the jejunal maximal transport rate for the uptake of glucose, and increased by over 150% ileal uptake of fructose. Protein abundance and mRNA expression of the sodium dependent glucose transporter in brush border membrane (SGLT1), sodium independent fructose transporter in the brush border membrane (GLUT5), sodium independent glucose and fructose transporter in the basolateral and brush border membranes (GLUT2), and Na(+)/K(+) ATPase alpha1 and beta1 did not explain the enhancing effect of budesonide on glucose or fructose uptake. Budesonide, prednisone, and dexamethasone reduced jejunal expression of the early response gene c-jun. In resected animals, expression of the mRNA of ornithine decarboxylase (ODC) in the jejunum was reduced, and corticosteroids reduced jejunal expression of the mRNA of proglucagon.


CONCLUSIONS
These data suggest that the influence of corticosteroids on sugar uptake in resected animals may be achieved by post translational processes involving signalling with c-jun, ODC, and proglucagon, or other as yet unknown signals. It remains to be determined whether budesonide may be useful to stimulate the absorption of sugars following intestinal resection in humans.
Thiesen
A
A
Nutrition and Metabolism Research Group, Division of Gastroenterology, Department of Medicine, University of Alberta, Edmonton, Canada.
Wild
G E
GE
Tappenden
K A
KA
Drozdowski
L
L
Keelan
M
M
Thomson
B K A
BK
McBurney
M I
MI
Clandinin
M T
MT
Thomson
A B R
AB
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D019819:Budesonide / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology; D005632:Fructose / Q000493:pharmacokinetics; D015870:Gene Expression; D005934:Glucagon / Q000032:analysis; D005947:Glucose / Q000493:pharmacokinetics*; D051273:Glucose Transporter Type 2; D051296:Glucose Transporter Type 5; D007082:Ileum / Q000187:drug effects / Q000378:metabolism*; D007408:Intestinal Absorption / Q000187:drug effects; D007421:Intestine, Small / Q000187:drug effects / Q000601:surgery; D007583:Jejunum / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D009004:Monosaccharide Transport Proteins / Q000032:analysis; D009955:Ornithine Decarboxylase / Q000032:analysis; D011241:Prednisone / Q000494:pharmacology; D052336:Proglucagon; D011498:Protein Precursors / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D051269:Sodium-Glucose Transporter 1; D000254:Sodium-Potassium-Exchanging ATPase / Q000032:analysis
D000893:Anti-Inflammatory Agents; D051273:Glucose Transporter Type 2; D051296:Glucose Transporter Type 5; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D011498:Protein Precursors; D012333:RNA, Messenger; C495676:Slc5a1 protein, rat; D051269:Sodium-Glucose Transporter 1; D005632:Fructose; D019819:Budesonide; D052336:Proglucagon; D003907:Dexamethasone; D005934:Glucagon; D009955:Ornithine Decarboxylase; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose; D011241:Prednisone