Apoptosis Participates in the Remodeling of the Endocrine Pancreas in the Neonatal Rat

Abstract

In rodents, shortly after birth a lack of increase in pancreatic weight and in islet mass have been reported during a time of overall body weight increase. To understand this regulation of the neonatal growth of the β cell mass, we studied Sprague Dawley rats at 2, 9, 13, 17, 20, 24, and 31 days of age for β cell replication, β cell mass, and cell size and for the presence of β cell apoptosis. β cell mass was stable from 2–20 days (range: 0.91 ± 0.2 to 1.33 ± 0.23 mg) and increased thereafter. β cell replication progressively decreased. Condensed apoptotic nuclei were identified and counted on paraffin sections using the fluorescent dye propidium iodide. Apoptoticβ cell nuclei were found at a basal rate (1.54 ± 0.22%) at 2, 9, and again after 20 days of age. However, at 13 and 17 days, the incidence of apoptosis was significantly increased (3.64 ± 0.45%). The decreased replication and the increased incidence of apoptosis in the β cells strongly suggest a wave of neogenesis of β cells to maintain the constant β cell mass. These data show that the endocrine pancreas undergoes significant modification during neonatal life and that apoptosis is an important mechanism in this remodeling of the β cell mass. Whether a selective deletion of some population ofβ cells occurs is unclear, but a dysregulation of this remodeling process could have important effects on the pancreatic β cell mass.