Abstract

GPR41 and GPR43 receptors are located at the level of the ileum and colon in the enteroendocrine cells, being activated by short-chain bacterial fatty acids, products of fermentation, these become a key to activate the mechanisms involved in this intestinal homeostasis. GPR43 and GPR41 mediate inflammatory processes such as colitis, but it has not been demonstrated their participation in vivo models of stress. In a model of acute and chronic restraint stress BALB/c mice we evaluated their expression. The measurement of serum corticosterone was performed to validate our model. Gene expression of Gpr41/Gpr43 through qPCR and protein expression of GPR41/GPR43 by Western Blot in both Large Intestine (IG) and Small Intestine (ID). Our results show that stress increases corticosterone levels being higher in chronic stress. Gene expression may show an increase for both receptors in chronic stress. Protein expression, unlike gene, has a greater increase in acute stress, except for GPR41 in ID where its increase is not significant. This suggests that an acute stimulation increases the expression of this receptor to conserve intestinal homeostasis, which initially deplete the gene machinery and then increase it by the constant appearance of the stressor stimulus although there seem to be post-translational mechanisms that do not allow. This shows us that the gradual increase of corticosterone apparently affects the expression of the protein of both receptors.

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