Objective:To analyze the correlation between sleep midpoint and sleep quality in insomnia patients with type 2 diabetes mellitus (T2DM).Methods:By adopting current situation investigation research, total of 150 T2DM patients hospitalized in the Department of Endocrinology, the First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine from November 2021 to July 2022 were selected as the research objects. The general information questionnaire, Pittsburgh Sleep Quality Index (PSQI), anxiety scale (SAS) and Depression Scale (SDS) were used to investigate, and then analysis the datum.Results:Among 150 T2DM insomnia patients, 41 cases (27.33%) were in the early midpoint sleep group, 37 cases (24.67%) were in the middle midpoint sleep group, and 72 cases (48.00%) were in the late midpoint sleep group. There were significant differences in the distribution of sex, age and BMI level among different sleep midpoint groups ( χ2=7.24, 13.36, 15.93, all P<0.05). The scores of time to fall asleep at the midpoint of sleep in the 3 groups were (2.12 ± 1.25), (2.65 ± 0.79), (2.33 ± 1.02), the difference was significant ( F=2.14, P<0.05); the daytime disability scores in the 3 groups were (1.39 ± 1.36), (2.16 ± 1.12), (1.85 ± 1.32), the difference was significant ( F=3.17, P<0.05). Logistic regression analysis of disorder showed that the time to fall asleep ( OR=4.922, P<0.05) and daytime disability ( OR=4.043, P<0.05) had significant influence to the middle midpoint of sleep group when the early midpoint of sleep group as the control, while the male ( OR=2.182, P<0.05), 50 - 70 years old ( OR=5.005, P<0.05) and BMI over fat side ( OR=3.488, P<0.05) had significant influence to the late midpoint of sleep group. Conclusions:Medical staff should pay attention to the sleep quality of T2DM patients, pay attention to the sleep midpoint of patients, and improve patients′cognition of healthy sleep patterns.

Dysregulation of circadian rhythms associates with cardiovascular disorders. It is known that deletion of the core circadian gene Bmal1 in mice causes dilated cardiomyopathy. However, the biological rhythm regulation system in mouse is very different from that of humans. Whether BMAL1 plays a role in regulating human heart function remains unclear. Here we generated a BMAL1 knockout human embryonic stem cell (hESC) model and further derived human BMAL1 deficient cardiomyocytes. We show that BMAL1 deficient hESC-derived cardiomyocytes exhibited typical phenotypes of dilated cardiomyopathy including attenuated contractility, calcium dysregulation, and disorganized myofilaments. In addition, mitochondrial fission and mitophagy were suppressed in BMAL1 deficient hESC-cardiomyocytes, which resulted in significantly attenuated mitochondrial oxidative phosphorylation and compromised cardiomyocyte function. We also found that BMAL1 binds to the E-box element in the promoter region of BNIP3 gene and specifically controls BNIP3 protein expression. BMAL1 knockout directly reduced BNIP3 protein level, causing compromised mitophagy and mitochondria dysfunction and thereby leading to compromised cardiomyocyte function. Our data indicated that the core circadian gene BMAL1 is critical for normal mitochondria activities and cardiac function. Circadian rhythm disruption may directly link to compromised heart function and dilated cardiomyopathy in humans.