Special Issue "New Insights into Gut Hormones and Intestinal Diseases"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Therapeutics".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 3304

Special Issue Editor

Dr. Hannelouise Kissow
E-Mail Website
Guest Editor
University of Copenhagen, Faculty of Health Sciences, Copenhagen, Denmark
Interests: gut

Special Issue Information

Dear Colleagues,

It has been evident for some years now that the intestinotrophic hormone glucagon-like peptide-2 (GLP-2) secreted from the entero-endocrine L cells, has therapeutic potential in treating intestinal diseases. Indeed, the GLP-2 analogue teduglutide is available for the treatment of short bowel syndrome. However, in recent years, it has been recognized that this is probably not the only hormone secreted from the gut implicated in either the pathogenesis or the adaptive and regenerating response in the intestines.

The anti-diabetic hormone glucagon-like peptide-1 (GLP-1) has been suggested both as a biomarker of intestinal damage and as a potential drug for the treatment of acute intestinal damage.

In this Special Issue, we wish to focus on all new aspects of the topic of gut hormones and intestinal diseases. Intestinal diseases in this setting include a wide range of conditions, such as short bowel syndrome, inflammatory bowel diseases, cancer, inherited diseases, and intestinal toxicities from other treatments. Suggested topics could be how intestinal disease influences the secretion of gut hormones; if and how these hormones contribute to the pathophysiology, and if the manipulation of gut hormone secretion modifies disease control.

Dr. Hannelouise Kissow
Guest Editor

Manuscript Submission Information

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Keywords

  • GLP-1
  • GLP-2
  • L-cell
  • intestines
  • short bowel syndrome
  • inflammatory bowel disease
  • mucositis
  • cancer

Published Papers (3 papers)

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Research

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Article
Pancreastatin Reduces Alternatively Activated Macrophages, Disrupts the Epithelial Homeostasis and Aggravates Colonic Inflammation. A Descriptive Analysis
Biomedicines 2021, 9(2), 134; https://doi.org/10.3390/biomedicines9020134 - 01 Feb 2021
Cited by 1 | Viewed by 835
Abstract
Ulcerative colitis (UC) is characterized by modifying alternatively activated macrophages (AAM) and epithelial homeostasis. Chromogranin-A (CHGA), released by enterochromaffin cells, is elevated in UC and is implicated in inflammation progression. CHGA can be cleaved into several derived peptides, including pancreastatin (PST), which is [...] Read more.
Ulcerative colitis (UC) is characterized by modifying alternatively activated macrophages (AAM) and epithelial homeostasis. Chromogranin-A (CHGA), released by enterochromaffin cells, is elevated in UC and is implicated in inflammation progression. CHGA can be cleaved into several derived peptides, including pancreastatin (PST), which is involved in proinflammatory mechanisms. Previously, we showed that the deletion of Chga decreased the onset and severity of colitis correlated with an increase in AAM and epithelial cells’ functions. Here, we investigated PST activity in colonic biopsies of participants with active UC and investigated PST treatment in dextran sulfate sodium (DSS)-induced colitis using Chga−/− mice, macrophages, and a human colonic epithelial cells line. We found that the colonic protein expression of PST correlated negatively with mRNA expression of AAM markers and tight junction (TJ) proteins and positively with mRNA expression of interleukin (IL)-8, IL18, and collagen in human. In a preclinical setting, intra-rectal administration of PST aggravated DSS-induced colitis by decreasing AAM’s functions, enhancing colonic collagen deposition and disrupting epithelial homeostasis in Chga+/+ and Chga−/− mice. This effect was associated with a significant reduction in AAM markers, increased colonic IL-18 release, and decreased TJ proteins’ gene expression. In vitro, PST reduced Chga+/+ and Chga−/− AAM polarization and decreased anti-inflammatory mediators’ production. Conditioned medium harvested from PST-treated Chga+/+ and Chga−/− AAM reduced Caco-2 cell migration, viability, proliferation, and mRNA levels of TJ proteins and increased oxidative stress-induced apoptosis and proinflammatory cytokines release. In conclusion, PST is a CHGA proinflammatory peptide that enhances the severity of colitis and the inflammatory process via decreasing AAM functions and disrupting epithelial homeostasis. Full article
(This article belongs to the Special Issue New Insights into Gut Hormones and Intestinal Diseases)
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Article
Intestinal Adaptation upon Chemotherapy-Induced Intestinal Injury in Mice Depends on GLP-2 Receptor Activation
Biomedicines 2021, 9(1), 46; https://doi.org/10.3390/biomedicines9010046 - 07 Jan 2021
Cited by 5 | Viewed by 803
Abstract
Intestinal adaptation is an important response and a natural repair mechanism in acute intestinal injury and is critical for recovery. Glucagon-like peptide 2 (GLP-2) has been demonstrated to enhance mucosal repair following intestinal damage. In this study, we aimed to investigate the role [...] Read more.
Intestinal adaptation is an important response and a natural repair mechanism in acute intestinal injury and is critical for recovery. Glucagon-like peptide 2 (GLP-2) has been demonstrated to enhance mucosal repair following intestinal damage. In this study, we aimed to investigate the role of GLP-2 receptor activation on intestinal protection and adaptation upon chemotherapy-induced intestinal injury. The injury was induced with a single injection of 5-fluorouracil in female GLP-2 receptor knockout (GLP-2R(-/-)) mice and their wild type (WT) littermates. The mice were euthanized in the acute or the recovery phase of the injury; the small intestines were analysed for weight changes, morphology, histology, inflammation, apoptosis and proliferation. In the acute phase, only inflammation was slightly increased in the GLP-2R(-/-) mice compared to WT. In the recovery phase, we observed the natural compensatory response with an increase in small intestinal weight, crypt depth and villus height in WT mice, and this was absent in the GLP-2R(-/-) mice. Both genotypes responded with hyperproliferation. From this, we concluded that GLP-2R signalling does not have a major impact on acute intestinal injury but is pivotal for the adaptive response in the small intestine. Full article
(This article belongs to the Special Issue New Insights into Gut Hormones and Intestinal Diseases)
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Review

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Review
GLP-1 and Intestinal Diseases
Biomedicines 2021, 9(4), 383; https://doi.org/10.3390/biomedicines9040383 - 05 Apr 2021
Cited by 4 | Viewed by 1215
Abstract
Accumulating evidence implicates glucagon-like peptide-1 (GLP-1) to have, beyond glucose maintenance, a beneficial role in the gastrointestinal tract. Here, we review emerging data investigating GLP-1 as a novel treatment for intestinal diseases, including inflammatory bowel diseases, short-bowel syndrome, intestinal toxicities and coeliac disease. [...] Read more.
Accumulating evidence implicates glucagon-like peptide-1 (GLP-1) to have, beyond glucose maintenance, a beneficial role in the gastrointestinal tract. Here, we review emerging data investigating GLP-1 as a novel treatment for intestinal diseases, including inflammatory bowel diseases, short-bowel syndrome, intestinal toxicities and coeliac disease. Possible beneficial mechanisms for these diseases include GLP-1′s influence on gastric emptying, its anti-inflammatory properties and its intestinotrophic effect. The current knowledge basis derives from the available GLP-1 agonist treatments in experimental animals and small clinical trials. However, new novel strategies including dual GLP-1/GLP-2 agonists are also in development for the treatment of intestinal diseases. Full article
(This article belongs to the Special Issue New Insights into Gut Hormones and Intestinal Diseases)
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