Gut microbiota and luminal dietary starch

The interaction between the gut microbiota and luminal dietary starch is a fundamental metabolic process that significantly influences human health. Dietary starch that escapes enzymatic digestion in the small intestine, known as resistant starch, reaches the colon where it serves as a primary substrate for fermentation by specific anaerobic bacteria, such as Ruminococcus bromii and Bifidobacterium species (Bird et al., 2010; Walker et al., 2011). This fermentation produces short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, which provide energy for colonocytes and function as systemic signaling molecules (Topping & Clifton, 2001). These metabolites play a crucial role in maintaining gut barrier integrity, modulating the immune system, and improving insulin sensitivity through the activation of host receptors like GPR41 and GPR43 (Koh et al., 2016). Dysregulation of this system is associated with various metabolic and inflammatory diseases, including obesity and inflammatory bowel disease. While not a single molecular target, this biological axis is modulated by drugs like acarbose, which increases the delivery of starch to the colon to promote beneficial microbial activity and improve glycemic control (Gu et al., 2017). Consequently, this system is a major focus for the development of prebiotic and probiotic therapies aimed at restoring metabolic homeostasis.

Other names

Resistant starch fermentationMicrobiome-starch interactionColonic starch degradationMicrobiota-accessible carbohydrates (MACs) metabolism

The interaction involves the microbial fermentation of undigested dietary starch (resistant starch) in the large intestine, primarily by specialized bacteria like Ruminococcus bromii. This process generates short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate, which act as signaling molecules by binding to G protein-coupled receptors (GPR41 and GPR43) and inhibiting histone deacetylases (HDACs) to regulate host inflammation and glucose metabolism (Koh et al., 2016; Walker et al., 2011).