The anthocyanins in black currants regulate postprandial hyperglycaemia primarily by inhibiting α-glucosidase while other phenolics modulate salivary α-amylase, glucose uptake and sugar transporters

Abstract

<p class="first" id="d1684592e107">The hypoglycaemic effects of two Ribes sp. i.e., anthocyanin-rich black currants (BC) were compared to green currants (GC), which are low in anthocyanins to establish which compounds are involved in the regulation of postprandial glycaemia. We determined the effect of the currants on inhibiting carbohydrate digestive enzymes (α-amylase, α-glucosidase), intestinal sugar absorption and transport across CaCo-2 cells. The digestion of these currants was modelled using in vitro gastrointestinal digestion (IVGD) to identify the metabolites present in the digested extracts by LC-MS/MS. Freeze-dried BC and IVDG extracts inhibited yeast α-glucosidase activity (P&lt;.0001) at lower concentrations than acarbose, whereas GC and IVDG GC at the same concentrations showed no inhibition. BC and GC both showed significant inhibitory effects on salivary α-amylase (P&lt;.0001), glucose uptake (P&lt;.0001) and the mRNA expression of sugar transporters (P&lt;.0001). Taken together this suggests that the anthocyanins which are high in BC have their greatest effect on postprandial hyperglycaemia by inhibiting α-glucosidase activity. Phytochemical analysis identified the phenolics in the currants and confirmed that freeze-dried BC contained higher concentrations of anthocyanins compared to GC (39.80 vs. 9.85 g/kg dry weight). Specific phenolics were also shown to inhibit salivary α-amylase, α-glucosidase, and glucose uptake. However, specific anthocyanins identified in BC which were low in GC were shown to inhibit α-glucosidase. In conclusion the anthocyanins in BC appear to regulate postprandial hyperglycaemia primarily but not solely by inhibiting α-glucosidase while other phenolics modulate salivary α-amylase, glucose uptake and sugar transporters which together could lower the associated risk of developing type-2 diabetes. </p>