RESUMO
We have previously reported that aqueous extract of gall from Rhus chinensis, known as "Obaeja", inhibited rat intestinal alpha-glucosidase and suppressed postprandial hyperglycemia by delaying digestion and absorption of intestinal carbohydrate (Shim et al., 2003). This led us to speculate that obaeja could be involved in ameliorating beta-cell injury by lowering glucotoxicity. In the present study, we thus examined the protective effect of obaeja on pancreatic beta-cell damage along with its anti-diabetic effect in streptozotocin-induced animal models. Streptozotocin was administered to rat pups (neonate/STZ model), or to adult rats with a lower dose using osmotic pump (osmotic pump/STZ model) for inducing beta cell death and diabetes. Obaeja was given to those rat pups after weaning in neonate/STZ model, or 2 weeks before subcutaneous implantation of osmotic pump to rats of the other latter model. In the diabetic control rats of the neonate/STZ model, which were not fed with obaeja, some pancreatic islets demonstrated a destruction of beta cell mass with insulitis 2 weeks after weaning, while some larger and irregular islets were formed by proliferation of alpha cells. In particular, we found some pancreatic lobules showing a severe inflammation and degeneration of islet and acinar tissues in this model. Islets in these inflammatory lobules were smaller in size with only few cells. In contrast, any inflammatory responses and insulitis were not observed in pancreas of the rats fed obaeja in this model. The islets in those rats maintained their normal profiles and islet cell population. Such anti-cytotoxic effect was also monitored in the diabetic rats of osmotic pump/STZ model. Especially, occurrence of hyperglycemia in the obaeja fed rats was delayed by 25~30 days than that of diabetic control rats in this model. Taken together, these results imply that regulation of postprandial blood glucose level by obaeja feeding may ameliorate a secondary injury caused by glucotoxicity.
