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Abstract
Anatomic alterations of the pancreas result in physiologic alterations that have not
been completely analyzed. Insulin plays a major role in carbohydrate metabolism; nevertheless,
as much as 50% of a hyperglycemic load may be metabolized independent of insulin.
We analyzed the effects of surgical alterations of the pancreas on postoperative glucose
metabolism, including insulin-independent effects. Mongrel female dogs underwent one
of three procedures: proximal partial pancreatectomy (PPx), PPx plus diversion of
pancreatic venous effluent to the systemic circulation (SC), or PPx plus segmental
pancreatic autotransplantation (PAT). Intravenous glucose tolerance tests, with or
without a background infusion of somatostatin (SST; 400 ng/kg/min) were performed
on all animals preoperatively and postoperatively. SST completely suppressed secretion
of assayable peripheral insulin. The rate of glucose disposal during SST suppression
approximates the rate of insulin-independent glucose disposal (IIGD). Although there
was a significant decrease in the rate of glucose disposal during SST infusion when
compared with the rate without SST, no differences in IIGD were found between postoperative
groups. IIGD was calculated at 50% to 55% for control, PPx, and SC groups and at 67%
for PAT. Peripheral sensitivity to an exogenous insulin infusion (euglycemic clamp)
was unchanged by any of the procedures. We conclude that surgical alteration of the
pancreas, including pancreas transplantation, results m altered glucose handling in
the face of “normal” peripheral levels of insulin. Changes in IIGD and analysis of
peripheral sensitivity to insulin do not explain these alterations completely.
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Article info
Publication history
Accepted:
November 18,
1988
Footnotes
☆Data in this article were presented in part at the Sixth International Symposium on Gastrointestinal Hormones, Vancouver, British Columbia, Canada, July 1986, and at the Clinical Congress of the American College of Surgeons, New Orleans, La., October 1986.
☆☆Supported by American Diabetes Research grant A 85-3249, University of Virginia Diabetes Research and Training Center feasibility grant, National Institutes of Health grant IR23 AM 35222-01A1 (J.B.H). Data handling made possible in part by NIH grant M01 RR 00847, University of Virginia General Clinical Research Center (D.L.K.). U-100 Regular Purified Peak insulin (Lot #6ED 61A) was supplied by the Eli Lilly Company, Indianapolis, Ind.
Identification
Copyright
© 1989 Published by Elsevier Inc.
