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Slowly digestible starch (SDS) is a functional carbohydrate fraction characterized by its complete but gradual digestion within the human small intestine, typically occurring between 20 and 120 minutes post-ingestion (Englyst et al., 1992). Unlike rapidly digestible starch (RDS), which causes sharp spikes in blood glucose and insulin, SDS provides a sustained and prolonged release of glucose into the bloodstream, resulting in a lower glycemic index and reduced insulin demand (Lehmann & Robin, 2007). This physiological profile makes SDS a critical dietary component for the management and prevention of metabolic disorders such as type 2 diabetes, obesity, and metabolic syndrome (Zhang & Hamaker, 2009). While SDS itself is a nutritional substrate rather than a traditional protein receptor or enzyme target, its breakdown is frequently the focus of pharmacological intervention using alpha-glucosidase inhibitors like acarbose, which further slow its conversion to glucose (Jenkins et al., 1981). The structural properties of SDS, such as high amylose content or specific semi-crystalline starch granules, dictate its resistance to rapid enzymatic hydrolysis by pancreatic alpha-amylase (Singh et al., 2010). Clinical monitoring of SDS efficacy typically involves measuring postprandial glucose levels and satiety markers over an extended period.
Slow enzymatic hydrolysis by pancreatic alpha-amylase and brush-border enzymes (maltase-glucoamylase and sucrase-isomaltase) in the small intestine, leading to a blunted and extended glucose absorption profile.
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