Journal of diabetes · 2025
Sleep Phenotypes, Genetic Susceptibility, and Risk of Obesity in Patients With Type 2 Diabetes: A National Prospective Cohort Study.
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Xi Lei, Li Li, Fu Songbo, Dai Yuancheng, Shi Juan, Yu Yanmei, Peng Ying, Qiu Hongmei, Kuang Jinsong, Lu Hongyun, Shao Huige, Yuan Chunlei, Wang Xiaohu, Zhang Ping, Li Sheli, Pan Yanhui, Hu Ling, Zhao Zhigang, Chen Yunxia, Kuang Jian, Shu Yi, Qian Jinhua, Mao Qibin, Zhang Jieji, Liu Yan, Yang Hong, Yan Zhaoli, Xie Weici, Zhang Qian, Zhang Ping, Wu Hongji, Gao Ling, Jin Yongjun, Xu Ning, Xu Chaoyang, Sun Xiaohui, Feng Zhimin, Zhang Qing, Li Lin, Ning Guang, Zhang Yifei, Cao Yanan, Wang Weiqing
Аннотация
BACKGROUND: To determine the associations between sleep phenotypes and the risks of specific obesity types and weight gain in patients with type 2 diabetes (T2D), especially in different genetic risk groups.
MATERIALS AND METHODS: We conducted a prospective study involving 58 890 participants. Sleep and napping were assessed according to the standardized questionnaire. General and abdominal obesity were defined by BMI or visceral fat area (VFA), respectively. Multivariable Cox regression, stratified, and joint analysis were performed to explore potential correlations. Furthermore, mediation models were constructed to figure out the mediating role of metabolic factors (blood pressure, UACR, and HbA1c).
RESULTS: During a median 3.05-year follow-up period, short sleep increased the risk of obesity (HR 1.42, 95% CI 1.17-1.71; 1.33, 1.08-1.65) and weight gain (1.21, 1.09-1.34; 1.17, 1.06-1.29), while long sleep and napping were unrelated to abdominal obesity and weight gain. Mediation analysis showed that systolic blood pressure, UACR, and HbA1c mediated the statistical association between night sleep duration and general obesity with proportions (%) of 7.9, 1.8, and 8.8, respectively. Joint analysis showed both sleep and napping groups had no significance among the low genetic risk group, while long napping, short sleep, and long sleep increased the risk of general obesity in medium to high risk patients.
CONCLUSIONS: Short sleep, long sleep, and long napping increased the risk of general obesity and BMI-defined weight gain, and were more pronounced in the medium to high genetic risk group. Napping was unrelated to abdominal obesity. Metabolic factors partially explain the mechanism between sleep and obesity.
MATERIALS AND METHODS: We conducted a prospective study involving 58 890 participants. Sleep and napping were assessed according to the standardized questionnaire. General and abdominal obesity were defined by BMI or visceral fat area (VFA), respectively. Multivariable Cox regression, stratified, and joint analysis were performed to explore potential correlations. Furthermore, mediation models were constructed to figure out the mediating role of metabolic factors (blood pressure, UACR, and HbA1c).
RESULTS: During a median 3.05-year follow-up period, short sleep increased the risk of obesity (HR 1.42, 95% CI 1.17-1.71; 1.33, 1.08-1.65) and weight gain (1.21, 1.09-1.34; 1.17, 1.06-1.29), while long sleep and napping were unrelated to abdominal obesity and weight gain. Mediation analysis showed that systolic blood pressure, UACR, and HbA1c mediated the statistical association between night sleep duration and general obesity with proportions (%) of 7.9, 1.8, and 8.8, respectively. Joint analysis showed both sleep and napping groups had no significance among the low genetic risk group, while long napping, short sleep, and long sleep increased the risk of general obesity in medium to high risk patients.
CONCLUSIONS: Short sleep, long sleep, and long napping increased the risk of general obesity and BMI-defined weight gain, and were more pronounced in the medium to high genetic risk group. Napping was unrelated to abdominal obesity. Metabolic factors partially explain the mechanism between sleep and obesity.