Abstract
Hyperglycemia is one of the main causes of diabetes complications. Gastrointestinal (GI) disturbances are one of the most frequent complications during diabetes. The porcine digestive tract possesses physiological and pathological similarities to the human digestive tract. This also applies to the innervation of the gastrointestinal tract. In this study, the influence of experimentally-inducted hyperglycemia was examined on the expression of vesicular acetylcholine transporter (VAChT), cocaine- and amphetamine-regulated transcript (CART), galanin (GAL), vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP) in the enteric nervous system (ENS) neurons in the small intestine of the pig. During the current study, an increased number of neurons containing CART, VIP, GAL, and CGRP under streptozotocin injection were observed. The augmentation of expression included all enteric plexuses present in the small intestine. The same results were obtained in the case of VAChT; namely, chronic hyperglycemia led to an increase in the number of neurons utilizing VAChT in all investigated plexuses. The obtained results suggested that the function of neuropeptides studied in this experiment depended on their localization in the ENS structures, as well as part of the GI tract. Diabetes led to alterations in the neurochemical phenotype of small intestine enteric neurons.
Highlights
The gastrointestinal (GI) tract is innervated by both the central nervous system (CNS) and by the enteric nervous system (ENS), located within the wall of the digestive tract [1]
The current study demonstrated the influence of chronically elevated glucose level, obtained as a result of streptozotocin injection, on the number of enteric neurons in the small intestine expressing selected neuropeptides in the pig as a model
We concluded that streptozotocin in a single dose (150 mg/kg) was able to induce diabetes in pig and suggested that STZ-injected pigs might serve as an essential model in early studies of pathological changes under hyperglycemic conditions in the peripheral nerve system
Summary
The gastrointestinal (GI) tract is innervated by both the central nervous system (CNS) and by the enteric nervous system (ENS), located within the wall of the digestive tract [1]. The ENS throughout the intramural plexuses (connected itself by a neuronal network) controls many digestive functions [1,2,3]. The ENS is characterized by high autonomy in the regulation of the GI tract function, but its functions may be regulated by CNS. The organization of the ENS clearly depends on the digestive tract region, but intraspecies differences have been observed [4,5,6]. The ENS in the small intestine contains several classes of neurons, including sensory neurons, interneurons, and motor neurons, through which smooth muscle activity, transmucosal fluid fluxes, local blood flow, nutrient resorption, and other functions are controlled and regulated. It should be stressed that the ENS controls gut functions independently from vago-vagal reflexes [8]
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