Plant-Derived Control of Postprandial Glycemia: α-Amylase, α-Glucosidase, and the Incretin-DPP-4 Interface

Abstract

Postprandial hyperglycemia can be modified before absorbed glucose reaches the circulation. Plant-derived compounds may slow starch hydrolysis through α-amylase and intestinal α-glucosidases, stimulate glucagon-like peptide-1 (GLP-1) release, or preserve incretin activity through dipeptidyl peptidase-4 (DPP-4) inhibition. This critical narrative review integrates these mechanisms around intestinal exposure, substrate selectivity, and human evidence. Flavonoids show structure-dependent and time-dependent inhibition of carbohydrate-hydrolyzing enzymes, but results vary markedly between yeast, rodent, and human enzyme systems. Iminosugar-rich mulberry preparations and thiosugar-containing Salacia extracts provide the strongest chemistry-to-clinic examples, including randomized trials that reduced postprandial glucose or HbA1c. Preclinical studies suggest that berberine may link bitter-taste-receptor-mediated GLP-1 secretion with local intestinal DPP-4 effects, whereas mangiferin, flavonol glycosides, anthocyanins, and food-derived peptides remain supported mainly by preclinical studies. In vitro potency alone is insufficient: meal composition, enzyme source, luminal concentration, metabolism, product standardization, gastrointestinal tolerance, and incretin measurements determine translational value. Candidate prioritization requires defined chemistry, achievable exposure, and product-specific human validation; acute effects do not establish durable benefit or human target engagement.