Intestinal Permeability to Glucose after Experimental Traumatic Brain Injury: Effect of Gadopentetate Dimeglumine Administration

Santos, Alejandro; Gonçalves, Pedro; Araújo, João Pedro; Martel, Fátima

doi:10.1111/j.1742-7843.2008.00272.x

Cited by 9 publications

(4 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Still, it is not clear yet, how the transepithelial transport of glucose is mediated under hypoxia. In spite of a reduced SGLT1 activity, the transepithelial transport of glucose has been reported to be stable under hypoxia [5,30], which was confirmed by the experiments presented herein (Figure 2). Looking for the transport mechanism responsible for sustaining the transepithelial transport of glucose, we used several inhibitors for flux measurements of 14 C-glucose (Figure 2).…”

Section: Discussionsupporting

confidence: 86%

“…Casting this aside, however, the most important finding of this experiment was an effect of STF-31, a GLUT1-inhibitor [33,34], under hypoxia only. This indicates that SGLT1 is indeed supplemented by another transport mechanism, i.e., GLUT1, although not by GLUT2 as postulated before [10,30,35]. This fits very well with GLUT1 gene transcription also being a HIF target [23], thus the long-term adaptation would support the modulations initiated in the short run.…”

Section: Discussionsupporting

confidence: 82%

See 1 more Smart Citation

The Fast Lane of Hypoxic Adaptation: Glucose Transport Is Modulated via A HIF-Hydroxylase-AMPK-Axis in Jejunum Epithelium

Dengler

Gäbel

2019

IJMS

View full text Add to dashboard Cite

The intestinal epithelium is able to adapt to varying blood flow and, thus, oxygen availability. Still, the adaptation fails under pathologic situations. A better understanding of the mechanisms underlying the epithelial adaptation to hypoxia could help to improve the therapeutic approach. We hypothesized that the short-term adaptation to hypoxia is mediated via AMP-activated protein kinase (AMPK) and that it is coupled to the long-term adaptation by a common regulation mechanism, the HIF-hydroxylase enzymes. Further, we hypothesized the transepithelial transport of glucose to be part of this short-term adaptation. We conducted Ussing chamber studies using isolated lagomorph jejunum epithelium and cell culture experiments with CaCo-2 cells. The epithelia and cells were incubated under 100% and 21% O2, respectively, with the panhydroxylase inhibitor dimethyloxalylglycine (DMOG) or under 1% O2. We showed an activation of AMPK under hypoxia and after incubation with DMOG by Western blot. This could be related to functional effects like an impairment of Na+-coupled glucose transport. Inhibitor studies revealed a recruitment of glucose transporter 1 under hypoxia, but not after incubation with DMOG. Summing up, we showed an influence of hydroxylase enzymes on AMPK activity and similarities between hypoxia and the effects of hydroxylase inhibition on functional changes.

show abstract

Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 82%

The Fast Lane of Hypoxic Adaptation: Glucose Transport Is Modulated via A HIF-Hydroxylase-AMPK-Axis in Jejunum Epithelium

Dengler

Gäbel

2019

IJMS

View full text Add to dashboard Cite

show abstract

“…Gut microbiota dysfunction is linked to brain disorders. Accumulating evidence has shown that TBI is a common occurrence following GI dysfunction, along with the secretion of pro‐inflammatory cytokines, degradation of intestinal TJ proteins, and increase in intestinal permeability . Previous studies have shown that SCFA‐producing bacteria could alleviate inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Clostridium butyricum exerts a neuroprotective effect in a mouse model of traumatic brain injury via the gut‐brain axis

Sun

et al. 2017

Neurogastroenterology Motil

126

View full text Add to dashboard Cite

show abstract

“…Rodent models of TBI recapitulate aspects of GI dysfunction seen in humans, including altered transit time 11 and increased intestinal permeability 5 , 12 . Such perturbations to normal GI function may result in disrupted nutrient absorption and bacterial translocation, potentially contributing to deleterious central nervous system outcomes 5 , 6 , 13 , 14 .…”

Section: Introductionmentioning

confidence: 99%

Acute gastrointestinal permeability after traumatic brain injury in mice precedes a bloom in Akkermansia muciniphila supported by intestinal hypoxia

DeSana,

Estus,

Barrett

et al. 2024

Sci Rep

View full text Add to dashboard Cite

Traumatic brain injury (TBI) increases gastrointestinal morbidity and associated mortality. Clinical and preclinical studies implicate gut dysbiosis as a consequence of TBI and an amplifier of brain damage. However, little is known about the association of gut dysbiosis with structural and functional changes of the gastrointestinal tract after an isolated TBI. To assess gastrointestinal dysfunction, mice received a controlled cortical impact or sham brain injury and intestinal permeability was assessed at 4 h, 8 h, 1 d, and 3 d after injury by oral administration of 4 kDa FITC Dextran prior to euthanasia. Quantification of serum fluorescence revealed an acute, short-lived increase in permeability 4 h after TBI. Despite transient intestinal dysfunction, no overt morphological changes were evident in the ileum or colon across timepoints from 4 h to 4 wks post-injury. To elucidate the timeline of microbiome changes after TBI, 16 s gene sequencing was performed on DNA extracted from fecal samples collected prior to and over the first month after TBI. Differential abundance analysis revealed that the phylum Verrucomicrobiota was increased at 1, 2, and 3 d after TBI. The Verrucomicrobiota species was identified by qPCR as Akkermansia muciniphila, an obligate anaerobe that resides in the intestinal mucus bilayer and produces short chain fatty acids (e.g. butyrate) utilized by intestinal epithelial cells. We postulated that TBI promotes intestinal changes favorable for the bloom of A. muciniphila. Consistent with this premise, the relative area of mucus-producing goblet cells in the medial colon was significantly increased at 1 d after injury, while colon hypoxia was significantly increased at 3 d. Our findings reveal acute gastrointestinal functional changes coupled with an increase of beneficial bacteria suggesting a potential compensatory response to systemic stress after TBI.

show abstract

Intestinal Permeability to Glucose after Experimental Traumatic Brain Injury: Effect of Gadopentetate Dimeglumine Administration

Cited by 9 publications

References 57 publications

The Fast Lane of Hypoxic Adaptation: Glucose Transport Is Modulated via A HIF-Hydroxylase-AMPK-Axis in Jejunum Epithelium

The Fast Lane of Hypoxic Adaptation: Glucose Transport Is Modulated via A HIF-Hydroxylase-AMPK-Axis in Jejunum Epithelium

Clostridium butyricum exerts a neuroprotective effect in a mouse model of traumatic brain injury via the gut‐brain axis

Acute gastrointestinal permeability after traumatic brain injury in mice precedes a bloom in Akkermansia muciniphila supported by intestinal hypoxia

Contact Info

Product

Resources

About