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Updated: Jun 26, 2026
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Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
Published on: November 9, 2018
Substance P, obesity, and gut inflammation
Iordanes Karagiannides1, Charalabos Pothoulakis
1Inflammatory Bowel Disease Center, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-7019, USA.
Current Opinion in Endocrinology, Diabetes, and Obesity
|December 24, 2008
Summary
Substance P may drive obesity by promoting fat tissue expansion, creating a pro-inflammatory state that can worsen gut inflammation, particularly in inflammatory bowel disease.
Area of Science:
- Neuroscience
- Immunology
- Gastroenterology
Background:
- Substance P is a neuropeptide involved in various physiological processes.
- Obesity and inflammatory bowel disease (IBD) are significant health concerns with complex etiologies.
- The interplay between metabolic and inflammatory conditions is an area of active research.
Purpose of the Study:
- To review recent data on substance P's effects on obesity and gut inflammation.
- To elucidate substance P's role in linking obesity and inflammatory responses in IBD.
- To explore substance P's potential as a therapeutic target.
Main Methods:
- Review of recent scientific literature and data.
- Analysis of studies investigating substance P's effects on adipose tissue.
- Examination of data on intestinal innervation changes during inflammation.
- Evaluation of studies on the impact of obesity on experimental colitis.
Main Results:
- Substance P directly influences fat tissue, affecting fat depot size and body weight in mice.
- Obesity exacerbates experimental colon inflammation in mice.
- Changes in substance P-positive sensory innervation are observed during gut inflammation.
- A potential link between substance P-mediated obesity and IBD progression is proposed.
Conclusions:
- Substance P may promote fat tissue expansion, leading to a pro-inflammatory environment that exacerbates gut inflammation.
- Further research is needed on the role of 'creeping fat' in IBD pathogenesis.
- Targeting substance P pathways could offer novel therapeutic strategies for obesity and IBD.
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