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Dietary starch and other digestible polysaccharides are complex carbohydrates that serve as the primary source of glucose for human energy metabolism [1]. These molecules, mainly composed of amylose and amylopectin, undergo enzymatic hydrolysis by salivary and pancreatic alpha-amylases, followed by further breakdown by brush-border alpha-glucosidases in the small intestine [2]. Although these polysaccharides are substrates rather than classical therapeutic targets like receptors or enzymes, their metabolic processing is a key site for pharmacological modulation [3]. Drugs such as acarbose and miglitol target the enzymes responsible for starch digestion, effectively slowing the rate of glucose absorption and mitigating postprandial blood sugar spikes [4]. This therapeutic approach is particularly relevant for managing Type 2 diabetes and improving glycemic control in patients with metabolic syndrome [5]. Consequently, while not a protein target, the regulation of starch digestion remains a cornerstone of nutritional and clinical interventions for metabolic health [6].
Inhibition of enzymatic hydrolysis by alpha-amylase and alpha-glucosidase to delay glucose absorption
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