Impaired neural pathway in gastric muscles of patients with diabetes

Abstract To explore the pathogenic mechanism of diabetic gastropathy, we investigated differences in response to electrical field stimulation (EFS) of gastric muscles from diabetic and non-diabetic (control) patients. Gastric specimens were obtained from 34 patients and 45 controls who underwent gas...

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Autores principales:	Yang Won Min, Eun-Ju Ko, Ji-Yeon Lee, Poong-Lyul Rhee
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/52808207c4764231a1bc047548687006
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spelling	oai:doaj.org-article:52808207c4764231a1bc0475486870062021-12-02T16:08:02ZImpaired neural pathway in gastric muscles of patients with diabetes10.1038/s41598-018-24147-y2045-2322https://doaj.org/article/52808207c4764231a1bc0475486870062018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-24147-yhttps://doaj.org/toc/2045-2322Abstract To explore the pathogenic mechanism of diabetic gastropathy, we investigated differences in response to electrical field stimulation (EFS) of gastric muscles from diabetic and non-diabetic (control) patients. Gastric specimens were obtained from 34 patients and 45 controls who underwent gastrectomy for early gastric cancer. Using organ bath techniques, we examined peak and nadir values of contraction under EFS. To examine responses to purinergic and nitrergic inhibition without cholinergic innervation, atropine, MRS2500, and N-nitro-L-arginine (L-NNA) were added sequentially to the organ bath. Tetrodotoxin (TTX) was used to confirm that the responses to EFS were mediated via neural stimulation. In the absence of pharmacological agents, peak contraction amplitude was greater in non-diabetic controls compared to diabetics only in the distal longitudinal gastric muscles. However, the nadir was greater in controls than in patients in both proximal and distal gastric circular muscles. Addition of MRS2500 could not decrease the nadir in both controls and patients, both in the proximal and distal stomach. However, L-NNA completely reversed the relaxation. TTX had no further effect on nadir. In conclusion, impaired inhibitory nitrergic neural pathway in both proximal and distal stomach and impaired excitatory cholinergic neural pathway in the distal stomach may contribute to the pathogenic mechanism underlying diabetic gastropathy.Yang Won MinEun-Ju KoJi-Yeon LeePoong-Lyul RheeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-9 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yang Won Min Eun-Ju Ko Ji-Yeon Lee Poong-Lyul Rhee Impaired neural pathway in gastric muscles of patients with diabetes
description	Abstract To explore the pathogenic mechanism of diabetic gastropathy, we investigated differences in response to electrical field stimulation (EFS) of gastric muscles from diabetic and non-diabetic (control) patients. Gastric specimens were obtained from 34 patients and 45 controls who underwent gastrectomy for early gastric cancer. Using organ bath techniques, we examined peak and nadir values of contraction under EFS. To examine responses to purinergic and nitrergic inhibition without cholinergic innervation, atropine, MRS2500, and N-nitro-L-arginine (L-NNA) were added sequentially to the organ bath. Tetrodotoxin (TTX) was used to confirm that the responses to EFS were mediated via neural stimulation. In the absence of pharmacological agents, peak contraction amplitude was greater in non-diabetic controls compared to diabetics only in the distal longitudinal gastric muscles. However, the nadir was greater in controls than in patients in both proximal and distal gastric circular muscles. Addition of MRS2500 could not decrease the nadir in both controls and patients, both in the proximal and distal stomach. However, L-NNA completely reversed the relaxation. TTX had no further effect on nadir. In conclusion, impaired inhibitory nitrergic neural pathway in both proximal and distal stomach and impaired excitatory cholinergic neural pathway in the distal stomach may contribute to the pathogenic mechanism underlying diabetic gastropathy.
format	article
author	Yang Won Min Eun-Ju Ko Ji-Yeon Lee Poong-Lyul Rhee
author_facet	Yang Won Min Eun-Ju Ko Ji-Yeon Lee Poong-Lyul Rhee
author_sort	Yang Won Min
title	Impaired neural pathway in gastric muscles of patients with diabetes
title_short	Impaired neural pathway in gastric muscles of patients with diabetes
title_full	Impaired neural pathway in gastric muscles of patients with diabetes
title_fullStr	Impaired neural pathway in gastric muscles of patients with diabetes
title_full_unstemmed	Impaired neural pathway in gastric muscles of patients with diabetes
title_sort	impaired neural pathway in gastric muscles of patients with diabetes
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/52808207c4764231a1bc047548687006
work_keys_str_mv	AT yangwonmin impairedneuralpathwayingastricmusclesofpatientswithdiabetes AT eunjuko impairedneuralpathwayingastricmusclesofpatientswithdiabetes AT jiyeonlee impairedneuralpathwayingastricmusclesofpatientswithdiabetes AT poonglyulrhee impairedneuralpathwayingastricmusclesofpatientswithdiabetes
_version_	1718384654828961792

Impaired neural pathway in gastric muscles of patients with diabetes

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