Publication: Glucose-mediated cytoprotection in the gut epithelium under ischemic and hypoxic stress
Authors
Huang, Chung Yen ; Pai, Yu Chen ; Yu, Linda Chia Hui
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia. Departamento de BiologĂa Celular e HistologĂa
publication.page.editor
publication.page.department
DOI
DOI: 10.14670/HH-11-839
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Single-layered intestinal epithelia play key
roles in the maintenance of gut homeostasis and barrier
integrity. Various types of epithelial cell death, including
apoptosis, necrosis, and necroptosis, have been detected
in ischemic and hypoxic stress conditions, thus resulting
in bacterial translocation and gut-derived septic
complications. Cytoprotective strategies, such as enteral
glucose uptake, rescue intestinal epithelium from cell
death after ischemic and hypoxic injury. Although
glucose metabolism and energy production are generally
considered to be the key factors in cytoprotection, the
precise modes and sites of action have not been clarified.
Our recent studies have demonstrated that energy
restoration promotes crypt hyperplasia but does not
prevent epithelial cell death under ischemic stress. On
the other hand, glycolytic pyruvate prevents epithelial
cells from undergoing apoptosis and necroptosis by
scavenging free radicals in an ATP-independent manner.
Distinct gut protective mechanisms involving ATP,
pyruvate, glucose metabolic enzymes, and sodiumdependent glucose transporter activation are discussed
here. Overall, glucose-mediated cytoprotection may be a
universal mechanism that has evolved in epithelial cells
for the maintenance of intestinal homeostasis. Enteral
glucose supplementation is beneficial as a perioperative
supportive therapy for the protection of gut barrier
integrity.
publication.page.subject
Citation
Histology and Histopathology, Vol.32, nÂş6, (2017)
item.page.embargo
Ir a EstadĂsticas
Este Ătem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/