Molecular Mechanism of Rectal Insulin Signalling in Inflammatory Bowel Disease
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 1617
Special Issue Editor
Interests: inflammatory bowel disease; rectal insulin treatment; insulin signaling in the colonocyte; intestinal development and morphogenesis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Intestinal epithelial cells harbor insulin receptors on their basolateral membranes. The physiological role of signaling through the insulin receptor in the intestinal epithelium remains elusive (if it exists at all). Mouse inactivation experiments have demonstrated that these insulin receptors do not play a role in intestinal development. However, under specific conditions, such as during high-fat diet-induced obesity, a phenotype can be elicited. Intriguingly, this phenotype includes changes in the number of certain enteroendocrine cells. In Ulcerative Colitis, insulin receptor mRNA can be upregulated in mucosal biopsies. Furthermore, immunohistochemistry revealed a correlation between this upregulation and increased amounts of insulin receptor immunoreactivity on the basolateral membranes of colonocytes. Subsequent experiments showed that rectally instilled insulin in mice with chemically induced colitis attenuated the inflammation. Collectively, these findings allow pharmacological targeting of epithelial insulin receptors using a local administration approach to treat inflammatory bowel diseases.
This Special Issue aims to compile original data and reviews that shed light on the molecular mechanisms underlying the anti-inflammatory effects observed with luminal insulin treatment. Papers exploring the effects of luminal insulin treatment on intestinal organoids or other cell types, such as enteroendocrine cells and even the microbiota, are also within the scope of this Special Issue.
Prof. Dr. Jørgen Olsen
Guest Editor
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Keywords
- inflammatory bowel disease
- insulin receptor
- enteroendocrine cells
- rectal insulin treatment
- inflammation
- microbiota
- differentiation
- local administration
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