Abstract

Abstract Objectives Retardation of starch digestion is an effective way of optimizing glycemic response. Certain bioactive food components inhibit starch digestion by binding with starch digestive enzymes or starch molecules in the digestive tract. Inclusion complexation between starch and guest compounds is a specific non-covalent binding mode and may contribute to a lower digestibility of starch. The aim of this study was to examine the inhibitory effects of alkyl gallates on in vitro starch digestion and the mechanism of inhibition. Methods Raw and cooked high amylose maize starch (HAMS) and potato starch (PS) were tested for in vitro enzymatic digestion. Gallic acid (GA) and alkyl gallates, including butyl (BG), octyl (OG), dodecyl (DG), hexadecyl (HG), and octadecyl (SG) gallates, were either added during digestion or processed to form inclusion complexes with starch prior to digestion. Starch digestibility profiles, represented by rapidly digestible starch (RDS), slowly digestible starch (SDS), and resistant starch (RS) contents, were determined. Results GA and alkyl gallates significantly increased (P < 0.05) RS content in raw starches. Cooked starches had significantly lower RS contents than raw starches. GA and BG increased RS content in cooked HAMS, while all compounds except for SG increased RS content in cooked PS. DG and HG caused a significant increase in SDS contents in cooked HAMS but not in raw starches and cooked PS. Significant increases in SDS and RS contents were seen in HAMS inclusion complexes with DG and HG, compared with uncomplexed starch. Conclusions The bioactive food components tested could all inhibit starch digestion either by inhibiting the enzymes or by forming starch inclusion complex. As alkyl chain length increased, their inhibition on enzymatic activity decreased, but their ability to bind starch increased. While cooking makes starch more digestible, adding certain bioactive food components could compensate for RS loss, suggesting a practical way of modulating glycemic response. Funding Sources USDA National Institute for Food and Agriculture.

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