Objective:To investigate the effect and possible mechanism of mammalian target of rapamycin (mTOR) protein and its related pathway on islet β cell proliferation in rats with chronic intermittent hypoxia (CIH). Methods:Twenty-four adult male Sprague-Dawley (SD) rats were randomly divided into two groups (the CIH group and the control group). The CIH group was fed in low oxygen cabins (60 s/N2 and 60 s/air alternately,oxygen concentrations between 5% and 21%,between 8:30~16:30 each day) for 35 days. We detected blood glucose and serum insulin levels by ELISA and calculated the insulin resistance index (HOMA-IR) and β cell insulin secretory function (HOMA-β) of the two groups. Glucose tolerance was evaluated by oral glucose tolerance test. The proliferation of pancreatic β cells was tested by immunofluorescence assay and mTOR and related pathway protein expressions were tested by Western blotting assays. Results:The fasting blood glucose,serum insulin levels and insulin resistance index increased (P < 0.01),while glucose tolerance and pancreatic β-cell function decreased (P < 0.05),in comparison with the control group. The number of ki67 positive β cells increased about five-fold while the mTOR related pathway protein expression of pancreatic tissues was activated. Conclusion:The rats in CIH condition showed insulin resistance,glucose tolerance impairment and pancreatic β-cell dysfunction;meanwhile,the activated mTOR pathway may play an important role in pancreatic β-cell proliferation.