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Intestinal Permeability to Glucose after Experimental Traumatic Brain Injury: Effect of Gadopentetate Dimeglumine Administration
Author(s) -
Santos Alejandro,
Gonçalves Pedro,
Araújo João R.,
Martel Fátima
Publication year - 2008
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00272.x
Subject(s) - traumatic brain injury , medicine , jejunum , intestinal permeability , intestinal mucosa , perfusion , gastroenterology , endocrinology , anesthesia , psychiatry
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.