title: Induction of 11beta-hydroxysteroid dehydrogenase type 2 and hyperaldosteronism are essential for enhanced sodium absorption after total colectomy in rats.
abstract: BACKGROUND
  Patients who undergo total colectomy with ileopouch anal reconstruction often have persistent diarrhea and frequent bowel movements. Analysis of the intestinal adaptation after total colectomy may lead to developing novel therapies for postoperative diarrhea.
  
  
  METHODS
  Sprague-Dawley rats underwent total colectomy with ileoanal reconstruction and were sacrificed 4 and 8 weeks later. Mucosal response to aldosterone was evaluated with the use of ileal mucosa in an Ussing chamber by measuring short circuit current after in vitro stimulation with aldosterone. We investigated the expression of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD 2) in intestinal epithelial cells. To examine the role of hyperaldosteronism, we also evaluated rats treated with a sodium-deficient diet or subcutaneous aldosterone infusion.
  
  
  RESULTS
  Aldosterone levels increased 80-fold after total colectomy. A comparable amount of aldosterone dramatically increased aldosterone-mediated, amiloride-sensitive short circuit current in the mucosa from colectomized rats, but not in control rats. We measured an increase in 11beta-HSD 2 messenger RNA and protein in the distal ileum from colectomized rats. Circulating aldosterone appears to be essential for these functional and molecular changes because similar results were obtained by using the mucosa from both dietary sodium-depleted and aldosterone-infused rats.
  
  
  CONCLUSIONS
  Induction of 11beta-HSD 2 is essential for enhanced mineralocorticoid action in the remnant ileum after total colectomy in rats.
authors.affiliation: Departments of Surgery and Pathology, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aoba-ku, Sendai 980-9574, Japan.
authors.forename: Shun
authors.initials: S
authors.lastname: Sato
authors.forename: Kouhei
authors.initials: K
authors.lastname: Fukushima
authors.forename: Hiroo
authors.initials: H
authors.lastname: Naito
authors.forename: Yuji
authors.initials: Y
authors.lastname: Funayama
authors.forename: Takashi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Hironobu
authors.initials: H
authors.lastname: Sasano
authors.forename: Zigmunt
authors.initials: Z
authors.lastname: Krozowski
authors.forename: Chikashi
authors.initials: C
authors.lastname: Shibata
authors.forename: Iwao
authors.initials: I
authors.lastname: Sasaki
mesh_terms: D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000235:genetics / Q000378:metabolism*; D000450:Aldosterone / Q000097:blood / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D003082:Colectomy; D039021:Colonic Pouches; D004232:Diuretics / Q000494:pharmacology; D004847:Epithelial Cells / Q000201:enzymology; D006929:Hyperaldosteronism / Q000378:metabolism*; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000166:cytology / Q000201:enzymology; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018161:Receptors, Mineralocorticoid / Q000235:genetics / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D012982:Sodium, Dietary / Q000494:pharmacology
chemical_list: D004232:Diuretics; D012333:RNA, Messenger; D018161:Receptors, Mineralocorticoid; D012982:Sodium, Dietary; D000450:Aldosterone; D000584:Amiloride; D012964:Sodium; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2