Objective To investigate brain functional abnormalities associated with the severity of insomnia in patients with depressive disorder using the cortical surface-based degree centrality. Methods A total of 317 patients with depressive disorder from 9 subcenters of the Depression Imaging REsearch ConsorTium （DIRECT） and 287 healthy controls were included in the study. Resting-state functional magnetic resonance imaging data were collected from all participants. The severity of depressive disorder in patients was evaluated using the 17-item Hamilton Depression Scale（ HAMD-17）. Patients were further divided into a high-insomnia group（ ≥ 4， n=202） and a low-insomnia group（ ≤ 3， n=115） based on the total scores of the HAMD-17 Insomnia Subscale. DPABISurf toolbox was used for data preprocessing and cortical surface-based degree centrality calculation. One-way covariance analysis was used to compare differences in cortical surface-based degree centrality among the high-insomnia group， low-insomnia group， and healthy control group. The degree centrality values of brain regions with statistically significant differences were extracted， and Spearman correlation was used to analyze the correlation between degree centrality and the severity of depressive disorder and insomnia in subgroups of patients with depressive disorder. Results There were no statistically significant differences in gender or mean framewise displacement among the three groups of participants（ all P＞0.05）. The age， adjusted HAMD-17 total score， and proportion of patients taking medication in the high-insomnia group were higher than those in the low-insomnia group， and the education years were lower than those in the healthy control group， with statistically significant differences（ all P＜0.05）. The cortical surface-based degree centrality of right Brodmann area 3b in the high-insomnia group and the low-insomnia group（ without global signal regression： F=16.35， P ＜ 0.001； with global signal regression： F=10.38， P ＜ 0.001） and the posterior pole of the right frontal lobe area 10（ without global signal regression： F=12.87， P＜0.001； with global signal regression： F=12.38， P＜ 0.001） was lower than that in the healthy control group， and these differences were statistically significant and were not affected by the global signal. There was no statistically significant difference in the cortical surfacebased degree centrality between the high-insomnia group and the low-insomnia group（ P＞ 0.05）. In the highinsomnia group， the degree centrality in right Brodmann area 3b was positively correlated with the adjusted HAMD-17 total score（ without global signal regression： r=0.19， P=0.006； with global signal regression： r=0.16， P=0.021）， and the difference was statistically significant. Conclusions Reduced cortical surfacebased degree centrality in the right Brodmann area 3b and the posterior pole of the right frontal lobe area 10 in patients with depressive disorder may reflect the core pathological feature of depressive disorder itself， rather than a state-dependent change associated with fluctuations in the severity of insomnia