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Exogenous leptin reinforces intestinal barrier function and protects from colitis
Belén Rivero-Gutiérrez1, Carlos J Aranda2, Borja Ocón1
1Department of Pharmacology, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), School of Pharmacy, Instituto de Investigación Biosanitaria Ibs, GRANADA, University of Granada, Granada, Spain.
Pharmacological Research
|July 30, 2019
Summary
Leptin administration reduced the severity of acute colitis in mice. This treatment reinforced intestinal mucosal barrier function, offering protection against dextran sulfate sodium-induced inflammation.
Area of Science:
- Gastroenterology
- Immunology
- Endocrinology
Background:
- Leptin regulates energy expenditure and food intake.
- Leptin's role in intestinal inflammation is debated, with conflicting reports of pro- and anti-inflammatory effects.
- Understanding leptin's impact on inflamed intestinal mucosa is crucial.
Purpose of the Study:
- To investigate the effect of exogenous leptin on acute experimental colitis.
- To evaluate leptin's influence on intestinal mucosal barrier function during inflammation.
Main Methods:
- C57BL/6 mice received exogenous PEG-leptin or saline for two weeks.
- Acute colitis was induced using dextran sulfate sodium (DSS) in drinking water after one week of treatment.
- Colitis severity, inflammatory markers, and mucosal barrier function were assessed.
Main Results:
- Leptin treatment significantly reduced colitis severity, evidenced by decreased rectal bleeding, epithelial damage, and inflammatory markers.
- Leptin administration improved diarrhea symptoms in DSS-induced colitis.
- Treated mice showed increased expression of tight junction proteins and proliferative markers, indicating enhanced mucosal barrier integrity.
Conclusions:
- Exogenous PEG-leptin confers protection in a DSS model of colitis.
- Leptin administration reinforces intestinal mucosal barrier function.
- Leptin may be a potential therapeutic agent for intestinal inflammation.
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