The present study extends preliminary investigations on the release of insulin-like activity (ILA) by pancreatic homografts.

Neonatal pancreas was implanted into the cheek pouch of alloxan-diabetic golden hamsters maintained with insulin. Hosts were treated additionally with cortisone and tolbutamide either singly or in combination. Homografts were evaluated structurally (aldehyde fuchsin) and functionally (fat pad bioassay) at periodic intervals.

In hosts receiving insulin alone, revascularization of the homografts occurred generally by seven days and complete exocrine degeneration by thirty days. The former process was delayed by cortisone and the latter accelerated by tolbutamide but delayed by cortisone. Cortisone prevented lymphocytic infiltration while tolbutamide significantly increased the number of islets with mitotic figures.

The number of homografts with islets demonstrating ILA in vitro was increased when hosts were pretreated with cortisone and insulin one week before transplantation and tolbutamide and insulin after transplantation. Arbitrary scoring of the survival and functional capacity of the homografts indicated this treatment to be twenty-eight times more effective than treatment with insulin alone. The magnitude of ILA released per transplant was not significantly different as a result of different treatments. However, omission of tolbutamide for twelve days prior to bioassay significantly increased the number of homografts able to release ILA. This suggests that the functional deficiencies observed with uninterrupted tolbutamide treatment may have resulted from overstimulation above that occurring as a consequence of diabetic hyperglycemia.

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