Objective To investigate the structural and functional changes of pancreas in D-galactose(D-gal)-induced aging mice. Methods Two-month-old male C57BL/6J mice were randomly divided into aging and control groups, 10 mice per group. The aging group was injected D-gal ［120 mg/(kg·d)］ for 42 days by continuous subcutaneous injection. The control group was injected saline with the same dosage. On the 2nd day after the aging model was established, the level of fasting blood glucose (FBG) and fasting insulin (FINS) in peripheral blood were detected. The body weight(g) and wet pancreatic weight(mg) were weighted to measure pancreas organ index. Microscopic structures of the pancreatic tissue were observed after HE staining. Frozen sections of pancreas were prepared to detect the aging ofsenescence-related β-galactosidase (SA-β-Gal) positive pancreas cells. Advanced glycation end products (AGEs) and its relative absorbance (RA) of pancreas tissue were assayed by immunohistochemistry. Superoxide dismutase (SOD), malonaldehyde (MDA) and total antioxidant capacity (T-AOC) in the pancreas tissue homogenate were assayed. Results Levels of FBG, pancreas wet weight and organ index in the aging group were significantly increased compared with the control group. The level of FINS was significantly decreased. Although the structural change of pancreas was not obvious, but the proportion of the area occupied by mononuclear cells in the pancreas islet was markedly increased. The contents of SOD and T-AOC were decreased and the level of MDA was increased in pancreatic tissue homogenate. Compared with the control group, the numbers of SA-β-Gal positive cells and the content of SOD and AGEs positive region were markedly increased in the aging group. Conclusion The structural and functional damages of pancreas exist in D-gal-induced aging mice. The mechanisms may be closely related to oxidative-stress damage.