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Feeding soybean resistant protein to rats raises fecal bile acid excretion but counteracts a deoxycholate-caused
N Azuma1, M Kanaya, R Kanamoto
1Department of Biological Resource Chemistry, Kyoto Prefectural University, Japan.
Journal of Nutritional Science and Vitaminology
|August 18, 1999
Summary
High-molecular-weight fraction (HMF) from soybean protein isolate enhances fecal lipid and steroid excretion, reducing colonic aberrant crypt foci (ACF) in rats. HMF may bind secondary bile acids, preventing colon exposure.
Area of Science:
- Gastroenterology
- Oncology
- Nutritional Science
Background:
- Azoxymethane (AOM) induces preneoplastic lesions in the rat colon.
- Deoxycholic acid (DCA) can influence the development of these lesions.
- Soybean protein isolate fractions are being investigated for their health effects.
Purpose of the Study:
- To investigate the effect of a high-molecular-weight fraction (HMF) from soybean protein isolate on azoxymethane-induced preneoplastic lesions in the rat colon.
- To determine if HMF influences fecal lipid and steroid excretion.
- To assess the interaction between HMF, deoxycholic acid (DCA), and colonic aberrant crypt foci (ACF) formation.
Main Methods:
- Male Fisher-344 rats were administered AOM and fed diets containing HMF or casein, with or without DCA supplementation.
- Growth parameters, fecal lipid, and acidic steroid excretions were measured.
- Colonic aberrant crypt foci (ACF) were quantified to assess preneoplastic lesion development.
Main Results:
- Feeding HMF diets significantly increased fecal lipid and acidic steroid excretions compared to casein diets.
- Secondary bile acids were prominent in the excreta of rats fed HMF.
- HMF intake reversed the effect of DCA on reducing ACF appearance, suggesting a protective role.
Conclusions:
- HMF, a fraction of soybean protein isolate, demonstrates potential in mitigating AOM-induced colonic preneoplastic lesions in rats.
- HMF enhances the excretion of lipids and secondary bile acids, potentially by binding them.
- This mechanism may prevent the interaction of harmful bile acids with the colonic mucosa, offering a protective effect against colon carcinogenesis.