Solute transporters and aquaporins are impaired in celiac disease

Umberto Laforenza, Emanuela Miceli, Giulia Gastaldi, Manuela F. Scaffino, Ulderico Ventura, Jacopo M. Fontana, Maria N. Orsenigo, Gino R. Corazza

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Background information. Celiac disease is a chronic inflammatory disorder of the small bowel induced in genetically susceptible subjects by gluten ingestion. Diarrhoea, weight loss and malabsorption represent the major clinical presentation of the disease. Here we examined the possible alteration in the expression and localization of water channels [AQPs (aquaporins)] and some solute transporters in duodenal mucosa of celiac disease patients. Duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls were considered in the present study. The expressions of some AQPs and transporter mRNAs in human duodenal biopsies were determined by semi-quantitative RT-PCR (reverse transcription PCR) and real-time RT-PCR. The localization of AQPs 3, 7 and 10 and of SGLT1 (Na+/glucose co-transporter 1), PEPT1 (H+/oligopeptide transporter 1) and NHE3 (Na+/H+ exchanger 3) was evaluated by immunohistochemistry. Results. AQPs 3, 7, 10 and 11, SGLT, PEPT and NHE, CFTR (cystic fibrosis transmembrane conductance regulator) and NKCC (Na-K-2Cl co-transporter) mRNAs were expressed in duodenal biopsies of healthy controls, treated celiac patients and disease controls. The expression of transcripts was virtually absent in duodenal biopsies of untreated celiac disease patients except for CFTR and NKCC. In healthy controls, immunohistochemistry revealed a labelling in the apical membrane of surface epithelial cells of the duodenum. The immunolabelling was heavily reduced or absent in untreated celiac patients, while it was normal in patients consuming a gluten-free diet for at least 12 months. Conclusions. Our results indicate that the main routes for water and solute absorption are deficient in celiac disease and may play a role in the onset of malabsorption symptoms.

Original languageEnglish
Pages (from-to)457-467
Number of pages11
JournalBiology of the cell / under the auspices of the European Cell Biology Organization
Volume102
Issue number8
DOIs
Publication statusPublished - 2010

Fingerprint

Aquaporins
Celiac Disease
Symporters
Abdomen
Biopsy
Cystic Fibrosis Transmembrane Conductance Regulator
Reverse Transcription
Immunohistochemistry
Gluten-Free Diet
Oligopeptides
Messenger RNA
Sodium-Hydrogen Antiporter
Facilitative Glucose Transport Proteins
Glutens
Duodenum
Weight Loss
Real-Time Polymerase Chain Reaction
Diarrhea
Mucous Membrane
Eating

Keywords

  • Aquaporin
  • Celiac disease
  • Cystic fibrosis transmembrane conductance regulator (CFTR)
  • Duodenal biopsy
  • Solute transporter

ASJC Scopus subject areas

  • Cell Biology
  • Medicine(all)

Cite this

Solute transporters and aquaporins are impaired in celiac disease. / Laforenza, Umberto; Miceli, Emanuela; Gastaldi, Giulia; Scaffino, Manuela F.; Ventura, Ulderico; Fontana, Jacopo M.; Orsenigo, Maria N.; Corazza, Gino R.

In: Biology of the cell / under the auspices of the European Cell Biology Organization, Vol. 102, No. 8, 2010, p. 457-467.

Research output: Contribution to journalArticle

Laforenza, Umberto ; Miceli, Emanuela ; Gastaldi, Giulia ; Scaffino, Manuela F. ; Ventura, Ulderico ; Fontana, Jacopo M. ; Orsenigo, Maria N. ; Corazza, Gino R. / Solute transporters and aquaporins are impaired in celiac disease. In: Biology of the cell / under the auspices of the European Cell Biology Organization. 2010 ; Vol. 102, No. 8. pp. 457-467.
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AU - Laforenza, Umberto

AU - Miceli, Emanuela

AU - Gastaldi, Giulia

AU - Scaffino, Manuela F.

AU - Ventura, Ulderico

AU - Fontana, Jacopo M.

AU - Orsenigo, Maria N.

AU - Corazza, Gino R.

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N2 - Background information. Celiac disease is a chronic inflammatory disorder of the small bowel induced in genetically susceptible subjects by gluten ingestion. Diarrhoea, weight loss and malabsorption represent the major clinical presentation of the disease. Here we examined the possible alteration in the expression and localization of water channels [AQPs (aquaporins)] and some solute transporters in duodenal mucosa of celiac disease patients. Duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls were considered in the present study. The expressions of some AQPs and transporter mRNAs in human duodenal biopsies were determined by semi-quantitative RT-PCR (reverse transcription PCR) and real-time RT-PCR. The localization of AQPs 3, 7 and 10 and of SGLT1 (Na+/glucose co-transporter 1), PEPT1 (H+/oligopeptide transporter 1) and NHE3 (Na+/H+ exchanger 3) was evaluated by immunohistochemistry. Results. AQPs 3, 7, 10 and 11, SGLT, PEPT and NHE, CFTR (cystic fibrosis transmembrane conductance regulator) and NKCC (Na-K-2Cl co-transporter) mRNAs were expressed in duodenal biopsies of healthy controls, treated celiac patients and disease controls. The expression of transcripts was virtually absent in duodenal biopsies of untreated celiac disease patients except for CFTR and NKCC. In healthy controls, immunohistochemistry revealed a labelling in the apical membrane of surface epithelial cells of the duodenum. The immunolabelling was heavily reduced or absent in untreated celiac patients, while it was normal in patients consuming a gluten-free diet for at least 12 months. Conclusions. Our results indicate that the main routes for water and solute absorption are deficient in celiac disease and may play a role in the onset of malabsorption symptoms.

AB - Background information. Celiac disease is a chronic inflammatory disorder of the small bowel induced in genetically susceptible subjects by gluten ingestion. Diarrhoea, weight loss and malabsorption represent the major clinical presentation of the disease. Here we examined the possible alteration in the expression and localization of water channels [AQPs (aquaporins)] and some solute transporters in duodenal mucosa of celiac disease patients. Duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls were considered in the present study. The expressions of some AQPs and transporter mRNAs in human duodenal biopsies were determined by semi-quantitative RT-PCR (reverse transcription PCR) and real-time RT-PCR. The localization of AQPs 3, 7 and 10 and of SGLT1 (Na+/glucose co-transporter 1), PEPT1 (H+/oligopeptide transporter 1) and NHE3 (Na+/H+ exchanger 3) was evaluated by immunohistochemistry. Results. AQPs 3, 7, 10 and 11, SGLT, PEPT and NHE, CFTR (cystic fibrosis transmembrane conductance regulator) and NKCC (Na-K-2Cl co-transporter) mRNAs were expressed in duodenal biopsies of healthy controls, treated celiac patients and disease controls. The expression of transcripts was virtually absent in duodenal biopsies of untreated celiac disease patients except for CFTR and NKCC. In healthy controls, immunohistochemistry revealed a labelling in the apical membrane of surface epithelial cells of the duodenum. The immunolabelling was heavily reduced or absent in untreated celiac patients, while it was normal in patients consuming a gluten-free diet for at least 12 months. Conclusions. Our results indicate that the main routes for water and solute absorption are deficient in celiac disease and may play a role in the onset of malabsorption symptoms.

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KW - Solute transporter

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