Abstract:Resistant starch (RS) resists digestion in the small intestine thus increasing the amount of starch available for microbial fermentation producing short chain fatty acids in the colon. Additionally, RS has been shown to reduce body fat in rodent models through mechanisms possibly related to colonic fermentation pathways. Acarbose, an α‐glucosidase inhibitor used to treat Type 2 diabetes, inhibits starch digestion in the small intestines, thus undigested starch reaches the colon mimicking the effects of RS. In … Show more
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