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Sodium butyrate does not decrease the evolution of precancerous lesions in rats
Fernanda Guimarães Drummond E Silva1, Luisa Costa Penna Penido, Flávia Xavier Valente
1UFV, Viçosa, MG, Brazil.
Acta Cirurgica Brasileira
|December 2, 2010
Summary
Sodium butyrate did not prevent aberrant crypt foci (ACF) in rats induced with 1,2-dimethylhydrazine (DMH). While spermidine and acetate levels changed, ACF formation was not inhibited, indicating no preventive effect against colorectal cancer progression.
Area of Science:
- Gastroenterology
- Oncology
- Nutritional Science
Background:
- Aberrant crypt foci (ACF) are early markers of colorectal cancer.
- Sodium butyrate, a short-chain fatty acid, has shown potential chemopreventive properties.
- Understanding the role of sodium butyrate in colorectal cancer prevention is crucial.
Purpose of the Study:
- To investigate the preventive efficacy of sodium butyrate against ACF formation.
- To assess the impact of sodium butyrate on colorectal carcinogenesis induced by 1,2-dimethylhydrazine (DMH).
Main Methods:
- Wistar rats were divided into control and sodium butyrate-treated groups.
- DMH was administered to induce colorectal cancer.
- Animals were observed for 4 or 8 weeks.
- ACF, polyamines, and short-chain fatty acid (SCFA) profiles were analyzed.
Main Results:
- Higher spermidine concentration was observed in the 8-week butyrate group compared to the control.
- Significant differences in acetate concentration were found between the 8-week control and butyrate groups.
- Sodium butyrate did not reduce the incidence or progression of ACF.
Conclusions:
- Sodium butyrate administration did not prevent ACF formation in DMH-induced colorectal cancer in rats.
- The study suggests sodium butyrate is ineffective in preventing colorectal cancer progression under these experimental conditions.
