Intestinal permeability to glucose after experimental traumatic brain injury: Effect of gadopentetate dimeglumine administration

• Type: Article in International Scientific Journal
• Date: 2008

Authors

Santos, Alejandro (Author) FCNAUP; Gonçalves P (Author) FMUP; Araújo JR (Author) FMUP; Martel, F (Author) FMUP

Journal

Title: Basic and Clinical Pharmacology and Toxicology

Vol. 103

Pages: 247-254

ISSN: 1742-7835

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 8 Citations

ISI Web of Science

Scopus - 10 Citations

Pubmed / Medline

Scientific classification

FOS: Medical and Health sciences > Health sciences

CORDIS: Health sciences

Other information

Authenticus ID: P-003-WC8

DOI: 10.1111/j.1742-7843.2008.00272.x

Abstract (EN): Traumatic injuries are the leading cause of mortality in individuals aged 1-44 years, and brain injury significantly contributes to the outcome in nearly one half of all deaths from trauma. At the intestinal level, traumatic brain injury (TBI) induces profound effects, including gastrointestinal mucosa ischaemia and motility dysfunction. However, nothing is known concerning the effect of TBI on the intestinal absorption of glucose. Hence, the aim of this study was to investigate the effect of TBI on the intestinal absorption of glucose by investigating the effect of TBI on the jejunal mucosal-to-serosal apparent permeability (AP-to-BL P(app)) to two glucose model substrates, (3)H-2-deoxy-D-glucose ((3)H-DG) and (3)H-3-O-methyl-D-glucose ((3)H-OMG), and to (14)C-sorbitol. Additionally, we tested if gadopentetate dimeglumine administration could prevent any of the changes observed after TBI. Traumatic brain injury induced an increase in the AP-to-BL P(app) to (3)H-DG. After a 100-min. perfusion of the jejunum, the AP-to-BL P(app) to (3)H-DG in TBI rats was almost 70% higher than in the control rats. There was no change, however, in the AP-to-BL P(app) to neither (3)H-OMG nor (14)C-sorbitol. Interestingly enough, gadopentetate dimeglumine was able to prevent the increase in the AP-to-BL P(app) to (3)H-DG observed after TBI. Given the differences in transport characteristics between (3)H-DG and (3)H-OMG, our results point to the possibility of the Na(+)-independent glucose transporter 2 (GLUT2) being activated by TBI (as the P(app) to (3)H-DG, a GLUT2 substrate, was increased) and the Na(+)-dependent glucose co-transporter (SGLT1) being inhibited by TBI (as the P(app) to (3)H-OMG, a GLUT2 and SGLT1 substrate, remained unchanged). Moreover, gadopentetate dimeglumine prevented these changes associated with TBI.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 8