Type 2 diabetes (T2D) is increasing rapidly in Africa. An appropriate therapeutic approach is to inhibit intestinal carbohydrate digesting enzymes using plant polyphenols. A crude preparation of sorghum condensed tannins (SCT) was highly effective (approx. 20,000 times) at inhibiting α-glucosidase compared to acarbose, while acarbose was a better α-amylase inhihitor (approx. 180 times). Kafirin microparticles (KEMS) were investigated as an oral delivery system for SCT. Using a simple aqueous alcohol coacervation method, the encapulation efficiency of SCT in the KEMS was approx. 48%. Quantitative data and electron microscopy revealed that KEMS encapsulating SCT were digested to only a limited extent during simulated gastrointestinal digestion with pepsin and trypsin-chymotrypsin.Hence, SCT encapsulated in KEMS retained their inhibitory activity against both amylases, throughout simulated gastrointestinal digestion, whereas unencapsulated SCT lost most of their inhibitory activity. Thus, KEMS encapsulating SCT have potential as a nutraceutical to attenuate hyperglycaemia and control T2D.

In vitro analysis has indicated that sorghum condensed tannins (SCT) survived simulated gastric digestion and inhibited digestive amylases when encapsulated in sorghum kafirin protein microparticles (SCT-KEMS). This study investigated SCT-KEMS as a potential antihyperglycaemic nutraceutical agent in vivo. Oral starch tolerance tests were performed on healthy rats. SCT-KEMS prevented a blood glucose spike and decreased the maximum blood glucose level by a mean of 11.8% compared to the water control, the same reduction as the acarbose standard. Neither SCT-KEMS nor acarbose elevated serum insulin levels. Further, the rats took the SCT-KEMS willingly,unlike the case with the unencapsulated SCTs. SCT-KEMS are potentially effective nutraceuticals for the management of hyperglycaemia because of the high affinity of SCT for the proline-rich kafirin and kafirin's slow digestibility, which enables SCT bitterness to be masked and delivered to the small intestine to inhibit carbohydrate hydrolysis, reducing glycaemic response.