Endocrine Abstracts

The magnitude and duration of postprandial blood glucose elevations due to hydrolysis of carbohydrates are major risk factors of diabetes and coronary heart diseases. Inhibition of the key carbohydrate hydrolyzing enzymes in the small intestine suppresses postprandial blood glucose peaks and reduces chronic vascular complications in diabetic subjects. Recent reports indicate that Syzygium spp-derived oleanolic acid (OA) inhibits glucose transport in the small intestine, but its effects on postprandial hyperglycaemia and key carbohydrate hydrolyzing enzymes remain unanswered. Accordingly, postprandial blood glucose variation was evaluated in non-diabetic and STZ-induced diabetic rats after loading with disaccharides (maltose and sucrose) and the polysaccharide, starch after 18-h fast with and without co-administration of OA. The inhibitory hydrolysis effects of OA against α-amylase, sucrase and α-glucosidase were also investigated in vivo and in-vitro. Rats administered with deionized water or acarbose acted as untreated and treated positive controls, respectively. By comparison with animals pre-loaded with carbohydrates alone, co-administration of OA with maltose, sucrose and starch significantly reduced the peak blood glucose spikes of separate groups of non-diabetic and STZ-induced diabetic rats. The standard drug, acarbose similarly suppressed the postprandial glucose spikes. The suppression of the postprandial glucose spikes response by OA to carbohydrate loads was associated with the reduction of the area under the blood glucose-time curve (AUC_{0.5–1 h}) of non-diabetic and diabetic animals. By comparison with untreated animals, OA significantly reduced the AUC_{0.5–1 h} of STZ-induced diabetic rats after loading with maltose (48.61±1.42 vs 36.87±0.91 mmol/l), sucrose (45.87±1.37vs 36.38±0.86 mmol/l) and starch (52.81±1.56 vs 40.95±1.33 mmol/l). The in vitro half-maximal inhibitory concentrations (IC₅₀) of OA on α-amylase, sucrase and α-glucosidase were 56.45±1.78, 59.88±1.35 and 62.11±1.79 μg/ml respectively. These results suggest that OA inhibits carbohydrate-hydrolyzing enzymes leading to suppression of postprandial hyperglycaemia in STZ-induced diabetic rats loaded with maltose, sucrose and starch.

Declaration of funding: This study was partly funded by the NRF South Africa and the University of KwaZulu-Natal, Research Division.