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Am J Physiol Endocrinol Metab 276: E822-E827, 1999;
0193-1849/99 $5.00
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Vol. 276, Issue 5, E822-E827, May 1999

Prior streptozotocin treatment does not inhibit pancreas regeneration after 90% pancreatectomy in rats

Diane T. Finegood1,2, Gordon C. Weir1, and Susan Bonner-Weir1

1 Elliot P. Joslin Research Laboratories, Joslin Diabetes Center, and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215; and 2 Diabetes Research Laboratory, School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6

The effects of residual beta -cell mass and glycemia on regeneration of endocrine pancreas after 90% pancreatectomy were investigated. Streptozotocin or buffer alone was injected into 4-wk-old male Lewis rats (day 0). On day 7, varying numbers of syngeneic islets were transplanted under the kidney capsule to achieve varying degrees of glucose normalization. On day 14, a 90% pancreatectomy or sham pancreatectomy was performed. On day 19, rats were killed and the pancreas was fixed for quantitative morphometric determination of beta -cell mass. Focal areas of regenerating pancreas were observed in all animals that underwent partial pancreatectomy. The percentage of remnant pancreas classified as foci was unaffected by streptozotocin treatment or by plasma glucose. Moderate to severe hyperglycemia did not promote regeneration of the pancreatic beta -cell mass; rather the total endocrine cell mass was inversely related to the plasma glucose level (r = -0.5, P < 0.01). These data suggest that the precursor population for both endocrine and exocrine tissue is not susceptible to damage by streptozotocin and that local effects of residual beta -cell mass are not important to regeneration after a 90% pancreatectomy.

islets of Langerhans; precursor cells


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