〔Abstract〕 Objective To investigate the expression of circular RNA(circRNA) circPRKDC in serum of patients with new-onset type 2 diabetes and its protective effect on palmitic acid-induced islet cell injury and its mechanism. Methods Fifty patients with new-onset type 2 diabetes and 50 healthy individuals who underwent physical examination during the same period were selected, and the expression of circPRKDC in serum was detected by real-time quantitative polymerase chain reaction(qRT-PCR).The mouse pancreatic β cell line MIN6 was treated with 110 μmol/L palmitic acid for 24 h to establish cell injury model.Negative control lentivirus or circPRKDC overexpression lentivirus were transfected, namely control group and circPRKDC group, respectively.Flow cytometry was used to determine the apoptosis and intracellular reactive oxygen species(ROS) levels of cells in each group.Bioinformatics software predicted miRNA with binding sites for circPRKDC.The dual-luciferase reporter gene experiment verified the direct binding of circPRKDC to downstream miRNA.The expression of miRNA in each group of cells was detected by qRT-PCR.Western blot was used to detect the expressions of apoptosis-related factors(Bax, Bcl-2,caspase 8) and inflammation-related proteins(NF-κB,p65) in each group of cells. Results Compared with healthy subjects, the expression of circPRKDC in serum of patients with type 2 diabetes was significantly lower(P<0.01).Compared with the control group, the expression of circPRKDC in the circPRKDC group increased(P<0.01),the level of apoptosis decreased(P<0.01),and the content of intracellular ROS decreased(P<0.01).circPRKDC directly bound miR-375(P<0.01).Compared with the control group, the expression of miR-375 in cells in the circPRKDC group decreased(P<0.01),the protein expression of Bcl-2 was up-regulated(P<0.01),and the protein expressions of Bax, caspase 8,NF-κB and p65 were down-regulated(allP<0.01). Conclusion The expression of circPRKDC is down-regulated in the serum of patients with new-onset type 2 diabetes, and it reduces palmitic acid-induced oxidative stress in islet cells by targeting miR-375,thereby inhibiting apoptosis and inflammatory responses.