title: Comparative study of epithelial gene expression in the small intestine among total proctocolectomized, dietary sodium-depleted, and aldosterone-infused rats.
abstract: We previously demonstrated enhanced plasma aldosterone, ileal activation of epithelial sodium channel (ENaC), and induction of 11 beta-hydroxysteroid dehydrogenase type 2 after total proctocolectomies in rats. However, factors other than circulating aldosterone may cause molecular induction associated with sodium transport. Sprague-Dawley rats were treated with sodium-deficient diets or subcutaneous aldosterone infusion for 4 weeks. Rats also underwent total proctocolectomies as positive control. We extracted epithelial RNA from the distal small intestine and compared mRNA expression of the alpha, beta, and gamma subunits of ENaC, prostasin, sodium glucose transporter 1 (SGLT1), and the alpha1 and beta1 subunits of Na(+)/K(+)-ATPase among control, total proctocolectomized, dietary sodium-depleted, and aldosterone-infused rats by quantitative reverse transcription-polymerase chain reaction or Northern blotting. A significant increase in aldosterone was noted in sodium-depleted and aldosterone-infused rats. The induction of three subunits of ENaC and prostasin mRNA was observed in proctocolectomized, aldosterone-infused rats but not in dietary sodium-depleted rats. The levels of the alpha1 and beta1 subunits of Na(+)/K(+)-ATPase were similar among the experimental groups. SGLT1 mRNA was induced only in proctocolectomized rats. The molecular induction of ENaC, prostasin, and SGLT1 is unique for total proctocolectomized rats. Aldosterone infusion can induce several essential molecules for sodium absorption, as seen in total proctocolectomy.
authors.affiliation: Department of Surgery, Tohoku University, Graduate School of Medicine, Sendai 980-8574, Japan. kouhei@surgl.med.tohoku.ac.jp
authors.forename: Kouhei
authors.initials: K
authors.lastname: Fukushima
authors.forename: Shun
authors.initials: S
authors.lastname: Sato
authors.forename: Hiroo
authors.initials: H
authors.lastname: Naito
authors.forename: Yuji
authors.initials: Y
authors.lastname: Funayama
authors.forename: Sho
authors.initials: S
authors.lastname: Haneda
authors.forename: Chikashi
authors.initials: C
authors.lastname: Shibata
authors.forename: Iwao
authors.initials: I
authors.lastname: Sasaki
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D003967:Diarrhea / Q000503:physiopathology*; D004847:Epithelial Cells / Q000502:physiology*; D053503:Epithelial Sodium Channels; D015870:Gene Expression; D006929:Hyperaldosteronism / Q000503:physiopathology*; D007150:Immunohistochemistry; D007421:Intestine, Small / Q000166:cytology*; D008297:Male; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D016737:Proctocolectomy, Restorative; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012697:Serine Endopeptidases / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology*; D051269:Sodium-Glucose Transporter 1; D000099271:Prostasin
chemical_list: D053503:Epithelial Sodium Channels; D008562:Membrane Glycoproteins; D009004:Monosaccharide Transport Proteins; D012697:Serine Endopeptidases; D015222:Sodium Channels; D051269:Sodium-Glucose Transporter 1; D000099271:Prostasin; C495676:Slc5a1 protein, rat