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Host digestive enzymes are a diverse group of catalytic proteins secreted by the salivary glands, stomach, pancreas, and small intestine to facilitate the chemical breakdown of dietary macronutrients into absorbable molecules [2, 13]. This group primarily includes amylases for carbohydrate digestion, lipases for lipid hydrolysis, and proteases, such as pepsin and trypsin, for protein degradation [13, 17]. These enzymes are essential for maintaining nutrient homeostasis; their deficiency, commonly observed in conditions like pancreatic exocrine insufficiency (PEI) or cystic fibrosis, leads to severe malabsorption and malnutrition [13, 17]. Pharmacologically, these enzymes are addressed through two main strategies: enzyme replacement therapy (ERT) to supplement endogenous deficiencies and enzyme inhibition to modulate metabolic processes [13, 18]. For example, alpha-glucosidase inhibitors are utilized to manage postprandial glycemia in type 2 diabetes, while lipase inhibitors like orlistat are used to treat obesity by reducing fat absorption [13]. Clinical monitoring often relies on biomarkers such as fecal elastase-1, and therapeutic use must be managed to avoid gastrointestinal side effects or rare complications like fibrosing colonopathy [1, 3].
Enzyme replacement therapy (exogenous supplementation of deficient enzymes) and competitive or non-competitive enzyme inhibition (reduction of nutrient absorption).
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