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

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.

Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System

“…5-hydroxytryptamine (5-HT) is a marker for EEC of the GI mucosa; small proportions of 5-HT cells also containing gastrin or SST can be found in the stomach, and glucagon-like peptide (GLP-1) or SST in the large intestine ( 34 ). SST-positive ( SST + ) neurons in the ENS are changed in pig diabetes model (Streptozotocin); SST + neurons increased only in the submucosal plexus in corpus of the stomach, and in the myenteric and submucosal plexus in all segments of the small intestine, but SST + neurons decreased in the descending colon ( 20 ). In female pig stomach, SST + immunoreactive neurons in the prepyloric area were increased in gastritis model (Aspirin, orally, 100mg/kg), in hyperacidity model (0.25MHCl intragastrical, 5ml/kg), and partial stomach resection model ( 21 ).…”