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The quantitative insulin response to glucose stimulus can be drastically reduced by subtotal pancreatectomy. An 80% pancreatectomy was performed preserving the pancreatic duct in seven dogs. The insulin output into the portal vein and cephalic vein insulin after intravenous glucose challenge were measured. Output was recorded in 25 controls, and before and 2 wk after subtotal pancreatectomy in the seven animals. Histologic sections of the original resection were compared with the remnant of pancreas taken at the end of the study. In this model, which approaches islet cell failure in terms of glucose homeostasis, the tactics that permit enhancement of islet function can be discerned and to some degree quantitated. The pancreatic remnant does not oversecrete to approximate normal function, although glucose sensitivity is somewhat enhanced. No beta-cell hyperplasia was seen. Despite low insulin output into the portal vein, systemic insulin levels are conserved. This decrease in the plasma clearance of insulin supports glucose homeostasis. Accommodation to severe islet reduction occurs via both intrapancreatic and, more importantly, extrapancreatic mechanisms.

A new method for the preparation of viable islet cells from the normal dog pancreas is described, based on the perfusion of the pancreatic duct with collagenase. Exposure of the acinar tissue to the highest concentrations of collagenase results in improved islet yield with decreased acinar contamination. After the selective digestion of the gland by ductal perfusion, mechanical dissociation liberates single cells and clumps. Analysis of the procedure by insulin yield and amylase attrition indicates a 57% B-cell recovery and a sixfold enrichment in B-cell concentration. The cells have been transplanted as autografts into dogs after pancreatectomy. In 5 of 7 transplanted dogs, normoglycemia was achieved postoperatively. DIABETES 30:455-458, May 1981.

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