摘要Background Growing evidence from population and clinic based studies showed that obstructive sleep apnea (OSA) and its characterizing chronic intermittent hypoxia (IH) were independently associated with the development of type 2 diabetes mellitus.However,the pathogenesis by which OSA induces glucose metabolic disorders is not clear.We determined changes in pancreatic β cell mass and the mammalian target of rapamycin (mTOR)/hypoxia inducible factor 1 (HIF-1)/ vascular endothelial growth factor A (VEGF-A) pathway following IH exposure.Methods A controlled gas delivery system regulated the flow of nitrogen and oxygen into a customized cage housing mice during the experiment.Twenty-four male wild C57BL/6J mice were either exposed to IH (n=12) or intermittent air as a control (n=12) for 56 days.Mice were anaesthetized and sacrificed after exposure,pancreas samples were dissected for immunofluorescent staining.Insulin and DAPI staining labelled islet β cells.Insulin positive area and β cell number per islet were measured.P-S6,HIF-1α and VEGF-A staining were performed to detect the activation of mTOR/HIF-1NEGF-A pathway.Results After eight weeks of IH exposure,insulin positive area increased by an average of 18.5％ (P ＜0.05).The β cell number per islet increased (92 vs.55,respectively for IH and the control groups,P ＜0.05) with no change in the size of individual β cells.Islet expression of HIF-1α and VEGF-A were higher in IH group than control group,and percentage of p-S6 positive β cell also increased after IH exposure (16.8％ vs.4.6％ respectively for IH and the control groups,P ＜0.05).Conclusion The number of pancreatic β cells increased as did the activity of the mTOR/HIF-1NEGF-A pathway after exposure to IH.