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Animal Models

Noise-induced sleep disruption increases weight gain and decreases energy metabolism in female rats

International Journal of Obesity (2018) | Download Citation




Inadequate sleep increases obesity and environmental noise contributes to poor sleep. However, women may be more vulnerable to noise and hence more susceptible to sleep disruption-induced weight gain than men. In male rats, exposure to environmental (i.e. ambient) noise disrupts sleep and increases feeding and weight gain. However, the effects of environmental noise on sleep and weight gain in female rats are unknown. Thus, this study was designed to determine whether noise exposure would disturb sleep, increase feeding and weight gain and alter the length of the estrous cycle in female rats.


Female rats (12 weeks old) were exposed to noise for 17d (8 h/d during the light period) to determine the effects of noise on weight gain and food intake. In a separate set of females, estrous cycle phase and length, EEG, EMG, spontaneous physical activity and energy expenditure were recorded continuously for 27d during baseline (control, 9d), noise exposure (8 h/d, 9d) and recovery (9d) from sleep disruption.


Noise exposure significantly increased weight gain and food intake compared to females that slept undisturbed. Noise also significantly increased wakefulness, reduced sleep and resulted in rebound sleep during the recovery period. Total energy expenditure was significantly lower during both noise exposure and recovery due to lower energy expenditure during spontaneous physical activity and sleep. Notably, noise did not alter the estrous cycle length.


As previously observed in male rats, noise exposure disrupted sleep and increased weight gain in females but did not alter the length of the estrous cycle. This is the first demonstration of weight gain in female rats during sleep disruption. We conclude that the sleep disruption caused by exposure to environmental noise is a significant tool for determining how sleep loss contributes to obesity in females.

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Funding for the publication was supported by the National Institutes of Health NS099468–01A1 (JAT), a CONICYT grant Fondecyt Regular 1150274 (CEP-L), and the USDA ARZT-1372540-R23–131 (JAT).

Author information


  1. Department of Nutritional Sciences, University of Arizona, Tucson, AZ, USA

    • Jamie E. Coborn
    • , Rebecca E. Lessie
    • , Christopher M. Sinton
    •  & Jennifer A. Teske
  2. Department of Pathology, University of Arizona, Tucson, AZ, USA

    • Naomi E. Rance
  3. Department of Neurology, University of Arizona, Tucson, AZ, USA

    • Naomi E. Rance
  4. College of Medicine, University of Arizona, Tucson, AZ, USA

    • Naomi E. Rance
  5. Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, AZ, USA

    • Naomi E. Rance
  6. Department of Physiology, School of Biological Sciences, Pontificia Universidad Catolica, Santiago, Chile

    • Claudio E. Perez-Leighton
  7. The Graduate Interdisciplinary Program in Physiological Sciences at the University of Arizona, Tucson, AZ, USA

    • Jennifer A. Teske
  8. The Graduate Interdisciplinary Program in Neuroscience at the University of Arizona, Tucson, AZ, USA

    • Jennifer A. Teske
  9. Department of Food Science and Nutrition at the University of Minnesota, Saint Paul, MN, USA

    • Jennifer A. Teske
  10. Minnesota Obesity Center at the University of Minnesota, Saint Paul, MN, USA

    • Jennifer A. Teske
  11. Minneapolis VA Health Care System, Minneapolis, MN, USA

    • Jennifer A. Teske


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The authors declare that they have no conflict of interest.

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Correspondence to Jennifer A. Teske.

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