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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 297/1/G116    most recent 90657.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Joly, F. Articles by Thomas, M. PubMed PubMed Citation Articles by Joly, F. Articles by Thomas, M.

MUCOSAL BIOLOGY

Morphological adaptation with preserved proliferation/transporter content in the colon of patients with short bowel syndrome

¹Service de Gastroentérologie et Assistance Nutritive, Pôle des Maladies de l'Appareil Digestif and ⁴Service d'Anatomo-pathologie, Hôpital Beaujon, Clichy; ²Unité d'Ecologie et de Physiologie du Système Digestif, UR 910, Institut National de la Recherche Agronomique, Jouy en Josas; ³Service d'Anatomo-pathologie, Hôpital Lariboisière, Paris, France

Submitted 16 November 2008 ; accepted in final form 2 April 2009

In short bowel syndrome (SBS), although a remaining colon improves patient outcome, there is no direct evidence of a mucosal colonic adaptation in humans. This prospective study evaluates morphology, proliferation status, and transporter expression level in the epithelium of the remaining colon of adult patients compared with controls. The targeted transporters were Na⁺/H⁺ exchangers (NHE2 and 3) and oligopeptide transporter (PepT1). Twelve adult patients with a jejuno-colonic anastomosis were studied at least 2 yr after the last surgery and compared with 11 healthy controls. The depth of crypts and number of epithelial cells per crypt were quantified. The proliferating and apoptotic cell contents were evaluated by revealing Ki67, PCNA, and caspase-3. NHE2, NHE3, PepT1 mRNAs, and PepT1 protein were quantified by quantitative RT-PCR and Western blot, respectively. In patients with SBS compared with controls, 1) hyperphagia and severe malabsorption were documented, 2) crypt depth and number of cells per crypt were 35% and 22% higher, respectively (P < 0.005), whereas the proliferation and apoptotic levels per crypt were unchanged, and 3) NHE2 mRNA was unmodified; NHE3 mRNA was downregulated near the anastomosis and unmodified distally, and PepT1 mRNA and protein were unmodified. We concluded that, in hyperphagic patients with SBS with severe malabsorption, adaptive colonic changes include an increased absorptive surface with an unchanged proliferative/apoptotic ratio and well-preserved absorptive NHE2, NHE3, and PepT1 transporters. This is the first study showing a controlled nonpharmacological hyperplasia in the colon of patients with SBS.

nutrition; colonic hyperplasia; proliferation markers; Ki67; PCNA; caspase-3; Na⁺/H⁺ exchanger 3; Na⁺/H⁺ exchanger 2; PepT1; hyperphagia