Intestinal resection- and steroid-associated alterations in gene expression were not accompanied by changes in lipid uptake.
OBJECTIVE
Glucocorticosteroids alter the morphology and transport function of the intestine of adult rats. This study was undertaken to assess the possible effect on intestinal lipid uptake of the locally acting steroid budesonide, or the systemically active prednisone or dexamethasone.


METHODS
Sprague-Dawley rats underwent intestinal transection or 50% intestinal resection. Budesonide, prednisone, dexamethasone, or control vehicle was given for 2 weeks from the time of surgery. Uptake was measured using ring uptake technique.


RESULTS
Resection had no effect on the mRNA expression for the early response genes, for proglucagon, or for the ileal lipid binding protein (ILBP), but was associated with reduced jejunal ornithine decarboxylase (ODC) mRNA and with reduced jejunal mRNA for the liver fatty acid binding protein (L-FABP). All three steroids reduced jejunal mRNA for proglucagon and c-jun, and did not affect the mRNA for L-FABP or for ILBP. These resection- and steroid-associated changes in gene expression were not associated with alterations in the intestinal uptake of long chain fatty acids or cholesterol.


CONCLUSIONS
The resection-associated alterations in the RNA expression of ODC and L-FABP and the steroid-associated changes in mRNA expression of c-jun and proglucagon were not accompanied by variations in lipid uptake.
Thiesen
A
A
Cell and Molecular Biology Collaborative Network in Gastrointestinal Physiology, University of Alberta, Edmonton, Canada.
Wild
G E
GE
Tappenden
K A
KA
Agellon
L B
LB
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; D019819:Budesonide / Q000494:pharmacology; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D015870:Gene Expression / Q000187:drug effects*; D005934:Glucagon / Q000235:genetics / Q000378:metabolism; D005938:Glucocorticoids / Q000494:pharmacology*; D007408:Intestinal Absorption / Q000187:drug effects*; D050356:Lipid Metabolism; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D029363:Organic Anion Transporters, Sodium-Dependent; D009955:Ornithine Decarboxylase / Q000235:genetics / Q000378:metabolism; D011241:Prednisone / Q000494:pharmacology; D052336:Proglucagon; D011498:Protein Precursors / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D027981:Symporters
D002352:Carrier Proteins; C493320:Fabp1 protein, mouse; C493321:Fabp1 protein, rat; C490174:Fabp7 protein, rat; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005938:Glucocorticoids; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D029363:Organic Anion Transporters, Sodium-Dependent; D011498:Protein Precursors; D012333:RNA, Messenger; D027981:Symporters; C071908:sodium-bile acid cotransporter; D019819:Budesonide; D052336:Proglucagon; D003907:Dexamethasone; D005934:Glucagon; D009955:Ornithine Decarboxylase; D011241:Prednisone