Effects of Creatine Treatment on Jejunal Phenotypes in a Rat Model of Acidosis

Abstract

We investigated the effects of creatine treatment on jejunal phenotypes in a rat model of oxidative stress induced by acidosis. In particular, the activities of some antioxidant enzymes (superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase), the level of lipid peroxidation, the expression of heat shock proteins (HSP70), and the expression of the major carriers of the cells (Na+/K+-ATPase, sodium-glucose Transporter 1—SGLT1, and glucose transporter 2—GLUT2) were measured under control and chronic acidosis conditions. Creatine did not affect the activity of antioxidant enzymes in either the control or acidosis groups, except for catalase, for which the activity was reduced in both conditions. Creatine did not change the lipid peroxidation level or HSP70 expression. Finally, creatine stimulated (Na+/K+)-ATPase expression under both control and chronic acidosis conditions. Chronic acidosis caused reductions in the expression levels of GLUT2 and SGLT1. GLUT2 reduction was abolished by creatine, while the presence of creatine did not induce any strengthening effect on the expression of SGLT1 in either the control or chronic acidosis groups. These results indicate that creatine has antioxidant properties that are realized through direct interaction of the molecule with reactive oxygen species. Moreover, the administration of creatine seems to determine a functional strengthening of the tissue, making it more resistant to acidosis.

Creatine Supplementation for Patients with Inflammatory Bowel Diseases: A Scientific Rationale for a Clinical Trial

“…Acidosis, associated with inflammatory conditions, produces oxidative stress and amplifies these effects, e.g., at an acidotic pH, the response of the intestine to an oxidative insult is magnified [ 33 ]. In a rat model of chronic acidosis, creatine supplementation was shown to exert direct anti-oxidant properties by directly scavenging ROS and creatine abolished the chronic reduction in the expression levels of glucose transporter (GLUT2) [ 34 ]. Moreover, the administration of creatine under chronic acidosis led to functional strengthening of this jejunal acidotic phenotype, making the tissue more resistant to acidosis [ 34 ].…”

“…In a rat model of chronic acidosis, creatine supplementation was shown to exert direct anti-oxidant properties by directly scavenging ROS and creatine abolished the chronic reduction in the expression levels of glucose transporter (GLUT2) [ 34 ]. Moreover, the administration of creatine under chronic acidosis led to functional strengthening of this jejunal acidotic phenotype, making the tissue more resistant to acidosis [ 34 ]. Thus, the beneficial influence and alleviation by creatine with respect to ischemic, oxidative and acidotic insults is certainly relevant for intestinal epithelial tissue, as well as for the entire intestine.…”