The Influence of a Hyperglycemic Condition on the Population of Somatostatin Enteric Neurons in the Porcine Gastrointestinal Tract

SIMPLE SUMMARY: Diabetes mellitus is a chronic metabolic disorder, in the course of which prolonged episodes of hyperglycemia are common. Hyperglycemia leads to damage and disruption in the proper function of many organs, including the gastrointestinal tract. Alimentary tract functions are regulated by triple innervation, in which the enteric nervous system plays a dominant role. Appropriate digestive functions are controlled by numerous biologically active substances which are synthesized and released through enteric neurons. One of the most common substances that occurs in the gastrointestinal tract is somatostatin. This peptide is involved in the regulation of a wide range of digestive functions, such as intestinal motility, secretory activity, and others. Furthermore, somatostatin participates in sensory and pain stimuli as well as modulation and release of other active factors. Somatostatin is also involved in the response of neurons to many pathological conditions. In this study, it was found that somatostatin secreted by enteric neurons has an important effect in hyperglycemic conditions induced by streptozotocin injection in the swine diabetes model. These data could provide useful information for further investigations into the functions of neuroactive substances in digestive tract pathophysiology in the course of diabetes. ABSTRACT: Somatostatin (SOM) is the most common agent in the gastrointestinal (GI) tract that is involved in the regulation of several gastric functions, as well as in gastric disorders. Hyperglycemia, which develops as a consequence of improperly treated diabetes, can cause numerous disturbances in the appropriate functioning of the gastrointestinal tract. High glucose level is toxic to neurons. One of the lines of defense of neurons against this glucotoxicity are changes in their chemical coding. To better understood the role of SOM secreted by enteric neurons in neuronal response on elevated glucose level, pancreatic β cells were destroyed using streptozotocin. Due to the close similarity of the pig to humans, especially the GI tract, the current study used pigs as an animal model. The results revealed that the number of enteric neurons immunoreactive to SOM (SOM-IR) in a physiological state clearly depend on the part of the GI tract studied. In turn, experimentally induced diabetes caused changes in the number of SOM-IR neurons. The least visible changes were observed in the stomach, where an increase in SOM-IR neurons was observed, only in the submucosal plexus in the corpus. However, diabetes led to an increase in the population of myenteric and submucosal neurons immunoreactive to SOM in all segments of the small intestine. The opposite situation occurred in the descending colon, where a decrease in the number of SOM-IR neurons was visible. This study underlines the significant role of SOM expressed in enteric nervous system neurons during diabetes.