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Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Université Paris 7, Paris-France
1Correspondence: Laboratoire de Physiopathologie de la Nutrition, CNRS ESA 7059, Tour 23–33-1er étage, 2, Place Jussieu, 75251 Paris Cedex 05 France.
We have investigated in adult rats made mildly diabetic by a low dose of streptozotocin (35 mg/kg; STZ rats) and in nondiabetic rats (ND rats) the mechanisms leading to adaptive changes in the ß cell mass, during glucose infusion and several days after stopping infusion. As early as 24 h of glucose infusion, the ß cell mass was maximally increased in ND and STZ rats. In both groups, this increase was due mainly to a rapid activation of neogenesis of new endocrine cells rather than to an increase in ß cell proliferation. Seven days after stopping glucose infusion, the ß cell mass returned to basal values in both groups as a result of stimulation of ß cell apoptosis and a decrease in ß cell replication rate. In glucose-infused ND rats, changes in the ß cell mass were correlated to insulin secretion, whereas in STZ rats, insulin secretion in response to glucose was still impaired whatever the ß cell mass. In conclusion, the data stress the impressive plasticity of the endocrine pancreas of adult rats. They also show that changes in ß cell mass in ND and STZ rats resulted from a disruption in the balance between neogenesis and apoptosis.—Bernard, C., Berthault, M.-F., Saulnier, C., Ktorza, A. Neogenesis vs. apoptosis as main components of pancreatic ß cell mass changes in glucose-infused normal and mildly diabetic adult rats.
Key Words: pancreas plasticity • streptozotocin • chronic hyperglycemia
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