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Chronic Insufficient Sleep in Women Impairs Insulin Sensitivity Independent of Adiposity Changes: Results of a Randomized Trial

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posted on 2023-11-03, 17:14 authored by Faris M. Zuraikat, Blandine Laferrère, Bin Cheng, Samantha E. Scaccia, Brooke Aggarwal, Sanja Jelic, Marie-Pierre St-Onge

Objective: Insufficient sleep is associated with type 2 diabetes (T2D), yet the causal impact of chronic insufficient sleep on glucose metabolism in women is unknown. We investigated whether prolonged mild sleep restriction (SR), resembling “real-world” short sleep, impairs glucose metabolism in women. Research Design and Methods: Women (20-75 y) without cardiometabolic diseases and with actigraphy-confirmed habitual total sleep time (TST) of 7-9 h/night were recruited to participate in this randomized, crossover study with two 6-wk phases: maintenance of adequate sleep (AS) and 1.5 h/night SR. Outcomes included plasma glucose, insulin, HOMA-IR from fasting blood draws as well as total area under the curve (AUC) for glucose and insulin, Matsuda index, and disposition index from an oral glucose tolerance test. Results: Our sample included 38 women (11 postmenopausal). Linear models adjusted for baseline outcome values demonstrated that TST was reduced by 1.34±0.04 h/night in SR vs. AS (p<0.0001). Fasting insulin (b=6.8±2.8 pmol/L, p=0.016) and HOMA-IR (b=0.30±0.12, p=0.016) were increased in SR vs. AS, with effects on HOMA-IR more pronounced in postmenopausal vs. premenopausal women (b=0.45±0.25 vs. b=0.27±0.13, p-interaction=0.042). Change in adiposity did not mediate the effects of SR on glucose metabolism or change results in the full sample when included as a covariate. Conclusions: Curtailing sleep duration to 6.2 h/night, reflecting the median sleep duration of US adults with short sleep, for 6 wk impairs insulin sensitivity, independent of adiposity. Findings highlight insufficient sleep as a modifiable risk factor for insulin resistance in women to be targeted in diabetes prevention efforts.

Funding

This clinical trial was supported by AHA grant 16SFRN27950012 (MPSO) and a NIH Clinical and Translational Science Award to Columbia University UL1TR001873. MPSO also receives support from NIH/NHLBI grants R01HL128226, R01DK128154, R35HL155670. FMZ is a Berrie Fellow in Diabetes and Obesity Research and is supported by NIH grants T32HL007343 and R01DK128154. BL is supported by NIH grants R01AG065569, P30DK063608, and R01DK128154. SJ is supported by AHA grant 16SFRN29050000 (SJ) and NIH grants R01HL106041 and R01HL137234. BA is supported by AHA grant AHA811531. The funding sources were not involved in study development, design, implementation, or dissemination.

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