In the intestine, gut distension and nutrients are detected by mechanoreceptors and chemoreceptors, respectively. The activation of these receptors sends an afferent nervous message to the hypothalamus in the brain. In turn, the hypothalamus controls the glucose entry in tissues, and thus glycemia.
Targeting the enteric nervous system that controls gut motility is now considered as an innovative therapeutic way in T2D to limit intestinal glucose absorption and restore the gut‐brain axis to improve insulin sensitivity. So far, little is known about the role of glucose on duodenal contraction in fasted and fed states in normal and diabetic conditions.
The enteric nervous system (ENS) plays a key role in controlling the gut-brain axis under normal and pathological conditions, such as type 2 diabetes. The discovery of intestinal actors, such as enterosynes, able to modulate the ENS-induced duodenal contraction is considered a pioneering approach.
In addition to their classical mode of action in the brain, circulating factors may modulate the release of reactive oxygen/nitrogen species (ROS/RNS) from endothelial cells that compose the blood-brain-barrier without entering the brain. Due to their high capacity to diffuse across membranes, ROS/RNS can reach neurons and modify their activity. This study investigates other mechanisms of actions in which beta-blockers may display a central effect without crossing the blood brain barrier.