Kolaviron modulates dysregulated metabolism in oxidative pancreatic injury and inhibits intestinal glucose absorption with concomitant stimulation of muscle glucose uptake.

This present study investigated the antioxidative and antidiabetic properties of kolaviron by analysing its inhibitory effect on key metabolic activities linked to T2D, in vitro and ex vivo. Kolaviron significantly inhibited α-glucosidase and α-amylase activities, and intestinal glucose absorption dose-dependently, while promoting muscle glucose uptake. Induction of oxidative pancreatic injury significantly depleted glutathione level, superoxide dismutase, catalase, and ATPase activities, while elevating malondialdehyde and nitric oxide levels, acetylcholinesterase and chymotrypsin activities. These levels and activities were significantly reversed in tissues treated with kolaviron. Kolaviron depleted oxidative-induced metabolites, with concomitant restoration of oxidative-depleted metabolites. It also inactivated oxidative-induced ascorbate and aldarate metabolism, pentose and glucuronate interconversions, fructose and mannose metabolism, amino sugar and nucleotide sugar metabolism, and arginine and proline metabolism, while reactivating selenocompound metabolism. These results depict the antidiabetic properties of kolaviron as indicated by its ability to attenuate oxidative-induced enzyme activities and dysregulated metabolisms, and modulated the enzyme activities linked to hyperglycaemia.