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The number of long‐term survivors of pancreatectomy for cancer is increasing. This study was conducted in patients with periampullary cancer to elucidate the serial change in the pancreatic endocrine functions before and after resection of the head of the pancreas. The pancreatic A and B cell functions were determined by the responses of plasma glucagon and insulin to arginine infusion. For serial comparison, the maximum response and integrated increment of plasma glucagon and insulin were calculated in each patient. There were no significant differences in these parameters between the patients (n=36) before the operation and normal controls (n=18). Early after pancreatoduodenectomy (mean, 6.4 weeks), each parameter was significantly less than its corresponding preoperative value and also less than the value in the normal controls. In the long‐term survivors (mean, 20.1 months after the surgery; n=12) among these 36 patients, these parameters showed no significant changes compared with the early postoperative values and were still significantly less than both the preoperative values and the normal control values. We, thus, conclude that pancreatic A and B cell functions are preserved long‐term after pancreatoduodenectomy in patients with periampullary cancer.

To elucidate the role of gastric inhibitory polypeptide (GIP) in the alteration of insulin secretion following pancreatoduodenal resection, in which the main sources of GIP are removed, plasma levels of GIP were measured for 180 minutes after oral glucose administration, both before and after radical pancreatoduodenectomy in nine patients with periampullary cancer. Fasting plasma levels of GIP remained much the same before and after surgery, and were not different from those in normal controls. The levels of GIP after glucose ingestion were significantly greater in the preoperative patients than in normal controls throughout 180 minutes. After pancreatoduodenectomy, the postglucose levels significantly diminished but remained within normal limits. Changes in plasma levels of insulin early after glucose ingestion in these patients, however, were significantly less both before and after surgery than in normal controls, and were not concomitant with the initial increase in plasma GIP. On the other hand, plasma levels of insulin greatly increased immediately after glucose ingestion in accordance with a rapid elevation of plasma GIP in 11 gastrectomized patients in whom the duodenum and the pancreas were preserved intact and who served as the control group. Thus, the diminution in GIP secretion following pancreatoduodenectomy may relate to the lack of main sources of this gut hormone and not to factors involved in the reconstruction of the alimentary tract. We conclude that the impaired insulin secretion following oral glucose ingestion in patients before and after pancreatoduodenectomy does not relate to the secretion of GIP.

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