Increased Expression of Mineralocorticoid Receptor in Human Ileum after Total Colectomy: Immunohistochemical and Immunoblotting Studies.

Abstract

Aldosterone is known to regulate transmembrane ion transport and water absorption through its binding to mineralocorticoid receptor (MR) in the mammalian colon. A possible roles of aldosterone has been suggested in increased water absorption from remnant ileum in the patients with total colectomy. We, therefore, studied immunolocalization of MR in remnant ileal mucosa in the patients with total colectomy in order to study the role of aldosterone in water and sodium absorption in these patients. Immunohistochemical localization of MR was performed in ileal mucosa of 7 patients with total colectomy and 5 cases of normal ileum obtained from the resection of ascending colon due to carcinoma by using a polyclonal antibody raised against a mineralocorticoid receptor fusion protein as a primary antibody and a biotinstreptavidin system for immunostaining. Immunoblotting was also performed. Positive MR immunoreactivity was observed in both cytoplasm and nucleus of absorptive cells of ileum of total colectomy patients but not in control normal ileum. Immunoblotting revealed the presence of an approximately 100 kDa immunoreactive product corresponding to mineralocorticoid receptor. Aldosterone is considered to act on ileal mucosa following total colectomy and the aldosterone dependent sodium transport and water absorption may be accelerated in ileal mucosa after total colectomy, which is consistent with the postoperative decrease in the stool volume observed in these patients. In conclusion, increased expression of the mineralocorticoid receptor in remnant ileum may play an important role in intestinal adaptation in total colectomized patients. mineralocorticoid receptor; immunohistochemistry; human intestine; total colectomy; intestinal adaptation

Metabolic cross talk between the colon and the periphery: implications for insulin sensitivity

“…TC not only leads to an increase in circulating aldosterone, but also up regulates GI expression of the mineralocorticoid receptor throughout the GI tract (Fukushima et al 1994). In addition, it increases expression (mRNA and protein) of the enzyme 11b-hydroxysteroid dehydrogenase type 2 (Sato et al 2005).…”