Objective Pancreatic endocrine cell neogenesis can be evaluated by quantifying the number of cells expressing the endocrine progenitor marker neurogenin3 (Neurog3). Neurog3-expressing cells are observed adjacent to the ductal structure in the embryonic pancreas, but few cells staining for Neurog3 persist after birth. Although this perinatal decline in Neurog3 is well recognized, its exact timing and mechanism are uncertain. Methods Using Neurog3-Timer mice in which DsRed-E5, a fluorescent protein that shifts its emission spectrum from green to red over time, is expressed transgenically in endocrine progenitors, we quantified the number of endocrine progenitors by flow cytometry. Results Endocrine neogenesis abruptly declined over the 24-hour period between embryonic day 18.5 (E18.5) and postnatal day 0.5 (P0.5). We hypothesized that signals associated with parturition control endocrine neogenesis, and tested whether inducing delayed delivery by progesterone administration in pregnant mice impacts the timing of the extinction of Neurog3 expression. Comparing E19.5 embryos with P0.5 newborn pups born at E19 revealed a preservation of Neurog3 expressing cells in the E19.5 embryos (0.80%) compared to P0.5 pups (0.21%), even though both groups were 19.5 days post coitus (dpc). Quantitative RT-PCR revealed that the P0.5 newborn pups also expressed much lower Neurog3 mRNA than E19.5 embryos. In contrast, pancreata from pups delivered one day early at 18.5 dpc due to induction with RU486, a progesterone receptor antagonist, had significantly smaller numbers of endocrine progenitors than normal E18.5 embryos. Conclusion These data demonstrate that signals associated with parturition tightly control pancreatic endocrine neogenesis.