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
Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, National Clinical Research Center for Metabolic Diseases (Shanghai), Ruijin Yangtze River Delta Health Institute, Research Unit of Clinical and Basic Research on Metabolic Diseases of Chinese Academy of Medical Sciences, Wuxi Branch of Ruijin Hospital, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Department of Endocrinology, The First Affiliated Hospital of Ningbo University, Ningbo, China.
J Diabetes. 2025 May;17(5):e70095. doi: 10.1111/1753-0407.70095.
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.
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).
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.
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.
确定2型糖尿病（T2D）患者的睡眠表型与特定肥胖类型及体重增加风险之间的关联，尤其是在不同遗传风险组中。
我们进行了一项前瞻性研究，纳入58890名参与者。根据标准化问卷评估睡眠和午睡情况。分别通过体重指数（BMI）或内脏脂肪面积（VFA）定义全身肥胖和腹型肥胖。进行多变量Cox回归、分层分析和联合分析以探索潜在相关性。此外，构建中介模型以明确代谢因素（血压、尿白蛋白肌酐比值和糖化血红蛋白）的中介作用。
在中位3.05年的随访期内，短睡眠增加了肥胖风险（风险比[HR] 1.42，95%置信区间[CI] 1.17 - 1.71；1.33，1.08 - 1.65）和体重增加风险（1.21，1.09 - 1.34；1.17，1.06 - 1.29），而长睡眠和午睡与腹型肥胖及体重增加无关。中介分析表明，收缩压、尿白蛋白肌酐比值和糖化血红蛋白分别以7.9%、1.8%和8.8%的比例介导了夜间睡眠时间与全身肥胖之间的统计学关联。联合分析表明，在低遗传风险组中，睡眠和午睡组均无显著意义，而在中高风险患者中，长时间午睡、短睡眠和长睡眠增加了全身肥胖风险。
短睡眠、长睡眠和长时间午睡增加了全身肥胖及BMI定义的体重增加风险，在中高遗传风险组中更为明显。午睡与腹型肥胖无关。代谢因素部分解释了睡眠与肥胖之间的机制。
