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. 2025 May;17(5):e70095.
doi: 10.1111/1753-0407.70095.

Sleep Phenotypes, Genetic Susceptibility, and Risk of Obesity in Patients With Type 2 Diabetes: A National Prospective Cohort Study

Lei Xi  1 , Li Li  2 , Songbo Fu  3 , Yuancheng Dai  4 , Juan Shi  1 , Yanmei Yu  5 , Ying Peng  1 , Hongmei Qiu  6 , Jinsong Kuang  7 , Hongyun Lu  8 , Huige Shao  9 , Chunlei Yuan  10 , Xiaohu Wang  11 , Ping Zhang  12 , Sheli Li  13 , Yanhui Pan  14 , Ling Hu  15 , Zhigang Zhao  16 , Yunxia Chen  17 , Jian Kuang  18 , Yi Shu  19 , Jinhua Qian  20 , Qibin Mao  21 , Jieji Zhang  22 , Yan Liu  23 , Hong Yang  24 , Zhaoli Yan  25 , Weici Xie  26 , Qian Zhang  27 , Ping Zhang  28 , Hongji Wu  29 , Ling Gao  30 , Yongjun Jin  31 , Ning Xu  32 , Chaoyang Xu  33 , Xiaohui Sun  1 , Zhimin Feng  1 , Qing Zhang  1 , Lin Li  1 , Guang Ning  1 , Yifei Zhang  1 , Yanan Cao  1   34 , Weiqing Wang  1
Affiliations

Sleep Phenotypes, Genetic Susceptibility, and Risk of Obesity in Patients With Type 2 Diabetes: A National Prospective Cohort Study

Lei Xi et al. J Diabetes. 2025 May.

Abstract

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.

Keywords: genetic risk; obesity; sleep; type 2 diabetes; weight gain.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Associations of different sleep phenotypes with weight gain among patients with type 2 diabetes. Weight gain was defined as an increase in BMI (A) or VFA (B) by more than 5%.
FIGURE 2
FIGURE 2
The joint association of night sleep duration (A), nap duration (B), and genetic risk of BMI with general obesity. The polygenic risk score for BMI (BMI‐PRS) was ranked from low to high.
FIGURE 3
FIGURE 3
Mediation analysis of metabolic factors on the relationship between night sleep duration and general obesity.
See this image and copyright information in PMC

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