The purpose of the present study was to investigate the changes in somatostatin release and somatostatin-containing D-cells of the stomach in streptozotocin (STZ)-induced diabetic rats after the amelioration of diabetes by whole pancreatic transplantation.
Highly inbred Lewis rats were divided in to three groups, (1) normal rats, (2) STZ-induced diabetic rats, and (3) diabetic-transplanted rats. Diabetes was induced by the administration of STZ (50 mg/kg). On the 7th day after STZ treatment, pancreatic transplantation was performed. Four weeks after the transplantation, in vivo and in vitro studies were performed. The in vivo studies revealed normalization of the elevated blood glucose and marked improvement of the impaired arginine-induced insulin release following the transplantation. The in vitro studies employing the isolated perfused rat stomachs revealed the following results. The mean basal gastric somatostatin release in the normal, diabetic and transplanted rats was 179±5, 173 plusmn;5 and 135±pg/m/, respectively. There was no significant difference between the normal and diabetic rats, although a significant decreased value was obtained in the transplanted rats (p<0.01 vs. normal, and p<0.01 vs. diabetic rats). On the other hand, the glucagon-stimulated peak somatostatin values in these groups were 498±36, 662+47, and 412±25 pg/m/, respectively. Glucagon-stimulated gastric somatostatin release in the diabetic rats was significantly increased, but reduced to normal values following pancreatic transplantation. The gastric somatostatin-containing D-cells were stained by an antibody-enzyme method. The number of gastric somatostatin-containing D-cells was markedly increased in the diabetic rats and decreased to normal levels in the transplanted rats.
In summary, enhanced gastric somatostatin release and increased D-cell number in the diabetic rats were both normalized after the amelioration of diabetes by whole pancreatic transplantation. From these results, it is suggested that gastric somatostatin is regulated by circulating insulin and/or metabolites of nutrients.