Certain low-digestible carbohydrates are utilized by gut microbiota mainly in the large intestine. Various molecules derived from the microbiota affect homeostasis of the host organism. Luminal nutrients stimulate the enteroendocrine system to secrete gut hormones in order to control physiological responses including gut motility, digestive enzyme secretion, nutrient absorption, glucose homeostasis, and appetite. Previous human and/or animal studies have demonstrated that continuous feeding of various low-digestible carbohydrates, including resistant maltodextrin (RMD), fructo-oligosaccharides (FOS), and difructose anhydride III promotes gut fermentation and secretion of glucagon-like peitde-1 (GLP-1)/peptide-YY (PYY). GLP-1 is an incretin hormone that improves glucose tolerance through enhancing insulin secretion from pancreatic beta cells and possibly through enhancing beta cell proliferation. PYY and GLP-1 have an anorexic effect which could prevent overeating. Gut fermentation products such as short-chain fatty acids increase the secretion of GLP-1 and PYY in the large intestine via activation of specific free-fatty acid receptors. Recent studies have shown that several other factors associated with gut microbiota could also be attributed to increased gut hormone secretions. In addition, our previous study revealed that RMD and FOS are able to directly activate GLP-1 secretion from enteroendocrine cells. Furthermore, we demonstrated that a rare sugar, D -allulose, potently stimulates GLP-1 secretion in rodent models. However, the molecular mechanisms underlying these phenomenons remain unknown and attract much research interest. This review summarizes the effects of low-digestible carbohydrates on enteroendocrine systems, the underlying mechanisms, and recent findings demonstrating direct/indirect effects of RMD and D -allulose on GLP-1 secretion.
Key word: low-digestible carbohydrates, enteroeodocrine systems, GLP-1, resistant maltodextrin, fructo-oligosaccharides, difructose anhydride III, D-allulose |
