In vitro and in vivo effects of sorghum condensed tannins encapsulated in kafirin microparticles on digestive amylases

Abstract

The International Diabetes Federation reported that by 2035 the expected increase in diabetes in sub-Saharan Africa will be 109%, the highest rise in the world. Furthermore, almost a quarter of the world‘s adult population have the metabolic syndrome. One therapeutic approach for type 2 diabetes (T2D) treatment is to inhibit digestive amylases and thereby decrease post-prandial hyperglycaemia. Polyphenols like sorghum condensed tannins (SCT) inhibit α-amylase and α-glucosidase enzymes. However, orally administered SCT may have poor inhibitory action against amylases, due to non-specific protein binding. Research is required to determine how to effectively deliver SCT to the small intestine to inhibit digestive amylases and decrease post-prandial hyperglycaemia. This study investigated the encapsulation of SCT in kafirin microparticles (KEMS) using aqueous ethanol and acetic acid coacervation methods. The inhibitory action of SCT on α- amylase and α-glucosidase were compared to acarbose (standard drug). The inhibition of SCT-KEMS after simulated gastrointestinal digestion was assessed. Electron microscopy was used to characterise microparticle morphology. A confirmatory in vivo test was performed using an oral starch tolerance test (OSTT) on healthy rats. SCT were about 20 000 times more effective at inhibiting α-glucosidase (IC50 = 0.4 μg/ml) than acarbose (IC50 = 8464.0 μg/ml), while acarbose (IC50 = 3.1 μg/ml) inhibited α-amylase better than SCT (IC50 = 554.5 μg/ml). The aqueous ethanol method of encapsulating SCT resulted in higher encapsulation efficiency (48%) than the acetic acid method (25%). Electron microscopy and quantitative data showed that SCT-KEMS were hardly digested by pepsin and trypsin-chymotrypsin during simulated digestion. SCT-KEMS retained their inhibitory activity against both amylases after simulated digestion, while SCT alone lost most of their inhibitory activity. In vivo data showed that the SCT-KEMS treatment decreased the maximum blood glucose level of rats by on average 11.8% and the area under the curve by 9%, compared to the water control. Acarbose decreased the blood glucose spike of the rats by on average 18.5% compared to the control. SCT-KEMS and acarbose did not elevate serum insulin levels and actually decreased insulin secretion by 60% and 48%, respectively, compared to the control. These findings indicate that KEMS are effective SCT encapsulating agents as they deliver the SCT to the small intestine. SCT-KEMS prevents hyperglycaemia by inhibiting digestive amylases and seems to substantially reduce insulin secretion when carbohydrate is consumed. Therefore, SCT-KEMS could be employed as a nutraceutical to inhibit digestive amylases and thereby attenuate post-prandial hyperglycaemia associated with the metabolic syndrome and T2D.