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The gut microbiota ecosystem and its interaction with dietary polysaccharides represent a complex symbiotic relationship essential for human metabolic and immunological health. Dietary polysaccharides, often termed microbiota-accessible carbohydrates (MACs), escape host digestion in the upper gastrointestinal tract and serve as the primary energy source for the colonic microbial community (Cell Metabolism, 2014). Through the process of fermentation, these microbes produce bioactive metabolites, most notably short-chain fatty acids (SCFAs) like butyrate, propionate, and acetate, which provide energy to colonocytes and act as systemic signaling molecules (Cell, 2016). This axis is a critical regulator of energy homeostasis, glucose metabolism, and the maintenance of the intestinal barrier (Cell Host & Microbe, 2018). Dysregulation of this ecosystem, frequently driven by low-fiber Western diets, is strongly associated with the development of chronic inflammatory and metabolic diseases, including obesity and inflammatory bowel disease (Science, 2016). While not a single molecular target, this system is therapeutically modulated through prebiotics, probiotics, and dietary interventions to restore microbial diversity and metabolic function (Gut Microbes, 2012). Drugs such as metformin and acarbose have also been shown to exert part of their therapeutic effect by altering the composition and metabolic output of this ecosystem (Nature Medicine, 2017).
Microbial fermentation of non-digestible polysaccharides into short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate, which subsequently activate host signaling pathways via G-protein coupled receptors (GPR41, GPR43, and GPR109A).
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