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Biomedicines
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Diabetes and Enteric Nervous System
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Diabetes and Enteric Nervous System

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 6260

Special Issue Editor

Dr. Nikolett Bódi

E-Mail Website
Guest Editor
Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary
Interests: enteric nervous system; diabetes; diabetic neuropathy; intestinal microbiota; animal models

Special Issue Information

Dear Colleagues,

Gastrointestinal symptoms related to diabetes refer to serious damage of enteric neurons and its environment. The enteric nervous system regulates all the gastrointestinal functions through its local reflex circuits, however the bidirectional communication between enteric and central nervous system is essential for fine modulation.

There is growing evidence that intestinal microbiota is especially susceptible to diabetic damage. Alterations of the microbial composition is critical in immune cell activation and trigger inflammatory processes contribute to enteric neuropathy. Investigation of the microbiota-gut-brain axis provides a new approach to study gastrointestinal and neurological disorders.

The aim of this Special Issue is to highlight the effects of diabetes on enteric nervous system and gastrointestinal tract or gut-brain axis. This Special Issue is open for original research articles as well as review articles. The elucidation of these aspects will contribute to understanding the development of diabetes-related neuronal damage and gastrointestinal injuries and provide basis to develop new therapeutic strategies.

Dr. Nikolett Bódi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • enteric nervous system
  • diabetes
  • bacterial dysbiosis
  • microbiota-gut-brain axis
  • neuroimmune interactions
  • neuronal environment
  • gastrointestinal motility

Published Papers (4 papers)

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Research

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11 pages, 707 KiB  
Article
Systemic Cytokine Expression in Diabetes Is Associated with Prolonged Gastrointestinal Transit Times and Cardinal Gastroparesis Symptoms
by Tina Okdahl, Anne-Marie Wegeberg, Anne Birthe Helweg Jensen, Sarah Thorius Jensen, Helene Riis Pontoppidan Andersen, Joachim Størling, Birgitte Brock and Christina Brock
Biomedicines 2023, 11(4), 1027; https://doi.org/10.3390/biomedicines11041027 - 27 Mar 2023
Cited by 1 | Viewed by 1113
Abstract
Gastroenteropathy is a common complication in diabetes associated with damages to the enteric nervous system. Systemic low-grade inflammation facilitates neurotoxicity, and associations with peripheral and autonomic neuropathy have been reported. However, less is known of associations with gastroenteropathy. To explore the area cross-sectionally, [...] Read more.
Gastroenteropathy is a common complication in diabetes associated with damages to the enteric nervous system. Systemic low-grade inflammation facilitates neurotoxicity, and associations with peripheral and autonomic neuropathy have been reported. However, less is known of associations with gastroenteropathy. To explore the area cross-sectionally, we included individuals with diabetes (type 1: 56, type 2: 100) and 21 healthy controls. Serum levels of interleukin (IL)-6, IL-8, IL-10, tumour necrosis factor (TNF)-α, and interferon (IFN)-γ were measured by multiplex technology. Segmental gastrointestinal transit times were assessed by wireless motility capsule investigations. Symptoms of gastroparesis were rated on Gastroparesis Cardinal Symptom Index questionnaires. Compared to healthy, levels of TNF-α were decreased in type 1 diabetes and increased in type 2 diabetes, while colonic transit time was increased (all p < 0.05). In diabetes, associations between IL-8 and prolonged gastric emptying (odds ratio (OR) 1.07, p = 0.027) and between IL-10 and prolonged colonic transit (OR 29.99, p = 0.013) were seen. Inverse correlations between IL-6 and nausea/vomiting (rho = −0.19, p = 0.026) and bloating (rho = −0.29; p < 0.001) were found. These findings indicate a plausible interaction between inflammation and the enteric nervous system in diabetes, which raises the question of whether anti-inflammatory strategies could be applied in management of diabetic gastroenteropathy. Full article
(This article belongs to the Special Issue Diabetes and Enteric Nervous System)
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15 pages, 7624 KiB  
Article
Intestinal Region-Dependent Alterations of Toll-Like Receptor 4 Expression in Myenteric Neurons of Type 1 Diabetic Rats
by Nikolett Bódi, Abigél Egyed-Kolumbán, Benita Onhausz, Bence Pál Barta, Afnan AL Doghmi, János Balázs, Zita Szalai and Mária Bagyánszki
Biomedicines 2023, 11(1), 129; https://doi.org/10.3390/biomedicines11010129 - 04 Jan 2023
Cited by 3 | Viewed by 1390
Abstract
Toll-like receptor 4 (TLR4) can activate pro-inflammatory cascades in the gastrointestinal tract. Our aim was to determine TLR4 expression in myenteric neurons of different gut regions using a type 1 diabetic model. Ten weeks after the onset of hyperglycemia, myenteric whole-mount preparations from [...] Read more.
Toll-like receptor 4 (TLR4) can activate pro-inflammatory cascades in the gastrointestinal tract. Our aim was to determine TLR4 expression in myenteric neurons of different gut regions using a type 1 diabetic model. Ten weeks after the onset of hyperglycemia, myenteric whole-mount preparations from the duodenum, ileum and colon of streptozotocin-induced diabetic, insulin-treated diabetic and control rats were prepared for TLR4/peripherin double-labelling fluorescent immunohistochemistry. Immunogold electron microscopy was applied to evaluate TLR4 expression in the myenteric perikaryon and neuropil. Tissue TLR4 levels were measured by enzyme-linked immunosorbent assay. In controls, the number and proportion of the TLR4-immunoreactive myenteric neurons showed an increasing tendency to aboral direction. These values were significantly higher in diabetics compared to controls in the duodenum and ileum, but were significantly lower in the colon. In diabetics, the distribution of TLR4-labelling gold particles between the perikaryon and neuropil of myenteric neurons varied in a different way by intestinal segment. TLR4 tissue concentration changed only in the diabetic duodenum, and it decreased in muscle/myenteric plexus-containing homogenates, while it increased in mucosa/submucosa/submucous plexus-containing samples relative to controls. Insulin had beneficial effects on TLR4 expression. These findings support that chronic hyperglycemia has segment-specific effects on TLR4 expression, contributing to gastrointestinal disorders in diabetic patients. Full article
(This article belongs to the Special Issue Diabetes and Enteric Nervous System)
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11 pages, 952 KiB  
Article
H19 and TUG1 lncRNAs as Novel Biomarkers for Irritable Bowel Syndrome in Diabetic Patients
by Marwa M. Esawy, Noorah Saleh Al-Sowayan, Maysa A. Mobasher, Amir Abd-elhameed, Elsayed S. Abd elbaser, Shereen A. Baioumy and Marwa A. Shabana
Biomedicines 2022, 10(11), 2978; https://doi.org/10.3390/biomedicines10112978 - 19 Nov 2022
Cited by 1 | Viewed by 1525
Abstract
Introduction: Irritable bowel syndrome (IBS) is a gastrointestinal disorder due to enteric nervous system impairment that produces different patterns of digestion. IBS is a common finding in diabetic patients. The functions of lncRNAs in IBS are still not clear and need to be [...] Read more.
Introduction: Irritable bowel syndrome (IBS) is a gastrointestinal disorder due to enteric nervous system impairment that produces different patterns of digestion. IBS is a common finding in diabetic patients. The functions of lncRNAs in IBS are still not clear and need to be further investigated. The aim of this study was to assess the diagnostic roles of lncRNA H19 and TUG1 for IBS associated with diabetes and to evaluate their association with clinical and laboratory findings. Subjects and Methods: Samples from 42 diabetic patients, 42 diabetic patients with IBS, and 42 healthy controls were obtained. The LncRNA H19 and TUG1 expressions were measured by quantitative real-time PCR. Results: The patients with IBS had significantly lower levels of lncRNA H19 and TUG1 expression than the healthy controls and diabetic-only patients (p < 0.001). LncRNA H19 and TUG1 can discriminate between diabetic-only patients and those with IBS (areas under the ROC curves of 0.95 and 0.722, respectively). The TUG1 expression levels were significantly different among types of IBS (IBS-D lower than IBS-M and IBS-C lower than IBS-M; p = 0.0165 and p = 0.043, respectively). H19 and TUG1 were downregulated in patients with poor glycemic control. lncRNA H19 and TUG1 expression in diabetic patients with IBS significantly negatively correlated with the IBS severity scoring system. Both lncRNAs’ expression significantly predicted the disease severity. LncRNA H19 expression can be an independent predictor for disease severity (adjusted odds ratio = 0.00001, 95% CI = 0–0.5, p = 0.045). Conclusions: Diabetic patients with IBS had significantly lower levels of lncRNA H19 and TUG1 expression than healthy controls and diabetic-only patients. LncRNA H19 had better diagnostic performance criteria for IBS. LncRNA H19 expression can be an independent predictor for IBS severity. Full article
(This article belongs to the Special Issue Diabetes and Enteric Nervous System)
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Review

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18 pages, 1016 KiB  
Review
Short-Chain Fatty Acids as Bacterial Enterocytes and Therapeutic Target in Diabetes Mellitus Type 2
by Maria-Adriana Neag, Anca-Elena Craciun, Andreea-Ioana Inceu, Diana-Elena Burlacu, Cristian-Ioan Craciun and Anca-Dana Buzoianu
Biomedicines 2023, 11(1), 72; https://doi.org/10.3390/biomedicines11010072 - 27 Dec 2022
Viewed by 1722
Abstract
Diabetes mellitus is a disease with multiple gastrointestinal symptoms (diarrhea or constipation, abdominal pain, bloating) whose pathogenesis is multifactorial. The most important of these factors is the enteric nervous system, also known as the “second brain”; a part of the peripheral nervous system [...] Read more.
Diabetes mellitus is a disease with multiple gastrointestinal symptoms (diarrhea or constipation, abdominal pain, bloating) whose pathogenesis is multifactorial. The most important of these factors is the enteric nervous system, also known as the “second brain”; a part of the peripheral nervous system capable of functioning independently of the central nervous system. Modulation of the enteric nervous system can be done by short-chain fatty acids, which are bacterial metabolites of the intestinal microbiota. In addition, these acids provide multiple benefits in diabetes, particularly by stimulating glucagon-like peptide 1 and insulin secretion. However, it is not clear what type of nutraceuticals (probiotics, prebiotics, and alimentary supplements) can be used to increase the amount of short-chain fatty acids and achieve the beneficial effects in diabetes. Thus, even if several studies demonstrate that the gut microbiota modulates the activity of the ENS, and thus, may have a positive effect in diabetes, further studies are needed to underline this effect. This review outlines the most recent data regarding the involvement of SCFAs as a disease modifying agent in diabetes mellitus type 2. For an in-depth understanding of the modulation of gut dysbiosis with SCFAs in diabetes, we provide an overview of the interplay between gut microbiota and ENS. Full article
(This article belongs to the Special Issue Diabetes and Enteric Nervous System)
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