Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Division of Sleep Medicine, Harvard Medical School, Boston, MA 02115, USA.
J Clin Endocrinol Metab. 2022 Jul 14;107(8):e3167-e3176. doi: 10.1210/clinem/dgac313.
Body fat gain associated with menopause has been attributed to estradiol (E2) withdrawal. Hypoestrogenism is unlikely to be the only contributing factor, however.
Given the links between sleep and metabolic health, we examined the effects of an experimental menopausal model of sleep fragmentation on energy metabolism.
Twenty premenopausal women (age 21-45 years) underwent a 5-night inpatient study during the mid-to-late follicular phase (estrogenized; n = 20) and the same protocol was repeated in a subset of the participants (n = 9) following leuprolide-induced E2 suppression (hypo-estrogenized). During each 5-night study, there were 2 nights of unfragmented sleep followed by 3 nights of fragmented sleep. Indirect calorimetry was used to assess fasted resting energy expenditure (REE) and substrate oxidation.
Sleep fragmentation in the estrogenized state increased the respiratory exchange ratio (RER) and carbohydrate oxidation while decreasing fat oxidation (all P < 0.01). Similarly, in the hypo-estrogenized state without sleep fragmentation, RER and carbohydrate oxidation increased and fat oxidation decreased (all P < 0.01); addition of sleep fragmentation to the hypo-estrogenized state did not produce further effects beyond that observed for either intervention alone (P < 0.05). There were no effects of either sleep fragmentation or E2 state on REE.
Sleep fragmentation and hypoestrogenism each independently alter fasting substrate oxidation in a manner that may contribute to body fat gain. These findings are important for understanding mechanisms underlying propensity to body fat gain in women across the menopause transition.
与绝经相关的体脂增加归因于雌二醇（E2）的撤退。然而，低雌激素血症不太可能是唯一的促成因素。
鉴于睡眠与代谢健康之间的联系，我们研究了实验性绝经睡眠碎片化模型对能量代谢的影响。
20 名绝经前妇女（年龄 21-45 岁）在中晚期卵泡期进行了 5 个晚上的住院研究（雌激素化；n=20），并在部分参与者（n=9）中重复了相同的方案，随后进行了促黄体生成素诱导的 E2 抑制（低雌激素化）。在每个 5 晚的研究中，有 2 个晚上进行无碎片化睡眠，然后进行 3 个晚上的碎片化睡眠。间接热量法用于评估空腹静息能量消耗（REE）和底物氧化。
在雌激素化状态下，睡眠碎片化增加了呼吸交换率（RER）和碳水化合物氧化，同时减少了脂肪氧化（均 P<0.01）。同样，在没有睡眠碎片化的低雌激素化状态下，RER 和碳水化合物氧化增加，脂肪氧化减少（均 P<0.01）；在低雌激素化状态下加入睡眠碎片化并没有产生除单独干预之外的进一步影响（P<0.05）。睡眠碎片化或 E2 状态对 REE 均无影响。
睡眠碎片化和低雌激素血症各自独立地改变了空腹底物氧化，这可能导致体脂增加。这些发现对于理解女性在绝经过渡期间体脂增加倾向的机制非常重要。
