Olfactory sensory neurons (OSNs) can regenerate after injury of the olfactory epithelium (OE). Insulin is a neural growth factor that plays important roles in neuronal survival and maturation. Insulin receptors are expressed both in the OE and olfactory bulb, but it is remains poorly understood how insulin signaling affects the regeneration of OSNs. We examined how insulin deficiency impedes the functional recovery of the OE after injury in adult mice using a type 1 diabetic mouse model. To induce type 1 diabetes, streptozotocin (STZ) was administered to selectively ablate pancreatic β cells, resulting in hypoinsulinemia. To injure the OE, methimazole, which induces apoptosis of OSNs was injected intraperitoneally. At day 7 after injury, no significant structural changes of the OE were observed between STZ- and control (saline-administered) mice. However, at day 14 and 28 after injury, remarkably fewer regenerated mature and more apoptotic OSNs were found in STZ-mice. STZ-mice showed smaller odorant-induced electroolfactogram (EOG) responses, a smaller number of c-Fos-positive cells in the olfactory bulb following odorant stimulation, and impaired performance in an odor-guided task at day 28 post-injury. Intranasal insulin administration during days 8 – 13 (unlike during days 0 – 6) after injury rescued the recovery of the OE in STZ-mice to levels similar in control mice. During day 8 – 13 after injury, insulin receptor expression was upregulated and the intranasal application of an insulin receptor antagonist slowed OE regeneration even in control mice. Furthermore, OE regeneration in control mice was enhanced by nasal insulin application during this period. These results suggest that newly generated OSNs have a high dependency on insulin signaling required for their maturation during the critical time window on days 8 – 13 after injury. Therefore, insulin signaling is a key factor for OE regeneration following injury.