ArticleAnimals : an open access journal from MDPI2020
The Influence of a Hyperglycemic Condition on the Population of Somatostatin Enteric Neurons in the Porcine Gastrointestinal Tract.
Article in Animals : an open access journal from MDPI, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Effects of Cholinergic and Opioid Antagonists on In Vitro Release of Met-Enkephalin, Somatostatin and Insulin-like Growth Factor-1 by and PENK Expression in Crop, Proventriculus and Duodenum of Newly Hatched Chickens.Animals : an open access journal from MDPI · 2025Article
- Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System.Frontiers in endocrinology · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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