Broussard Josiane L, Chapotot Florian, Abraham Varghese, Day Andrew, Delebecque Fanny, Whitmore Harry R, Tasali Esra
Diabetes and Obesity Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd, THA E104, Los Angeles, CA, 90048, USA,
Diabetologia. 2015 Apr;58(4):791-8. doi: 10.1007/s00125-015-3500-4. Epub 2015 Feb 22.
AIMS/HYPOTHESIS: Sleep loss is associated with insulin resistance and an increased risk for type 2 diabetes, yet underlying mechanisms are not understood. Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Circulating NEFA in healthy individuals shows a marked diurnal variation with maximum levels occurring at night, yet the impact of sleep loss on NEFA levels across the 24 h cycle remains unknown. We hypothesised that sleep restriction would alter hormones that are known to stimulate lipolysis and lead to an increase in NEFA levels.
We studied 19 healthy young men under controlled laboratory conditions with four consecutive nights of 8.5 h in bed (normal sleep) and 4.5 h in bed (sleep restriction) in randomised order. The 24 h blood profiles of NEFA, growth hormone (GH), noradrenaline (norepinephrine), cortisol, glucose and insulin were simultaneously assessed. Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test.
Sleep restriction relative to normal sleep resulted in increased NEFA levels during the nocturnal and early-morning hours. The elevation in NEFA was related to prolonged nocturnal GH secretion and higher early-morning noradrenaline levels. Insulin sensitivity was decreased after sleep restriction and the reduction in insulin sensitivity was correlated with the increase in nocturnal NEFA levels.
CONCLUSIONS/INTERPRETATION: Sleep restriction in healthy men results in increased nocturnal and early-morning NEFA levels, which may partly contribute to insulin resistance and the elevated diabetes risk associated with sleep loss.
目的/假设:睡眠不足与胰岛素抵抗及2型糖尿病风险增加有关,但其潜在机制尚不清楚。循环中非酯化(即游离)脂肪酸(NEFA)浓度升高可导致胰岛素抵抗,并在代谢性疾病的发展中起核心作用。健康个体的循环NEFA呈现明显的昼夜变化,夜间水平最高,但睡眠不足对24小时周期内NEFA水平的影响仍不清楚。我们假设睡眠限制会改变已知刺激脂肪分解的激素,并导致NEFA水平升高。
我们在受控的实验室条件下对19名健康年轻男性进行了研究,他们随机连续四晚分别卧床8.5小时(正常睡眠)和4.5小时(睡眠限制)。同时评估NEFA、生长激素(GH)、去甲肾上腺素、皮质醇、葡萄糖和胰岛素的24小时血液变化情况。通过频繁采样的静脉葡萄糖耐量试验评估胰岛素敏感性。
与正常睡眠相比,睡眠限制导致夜间和清晨时段NEFA水平升高。NEFA的升高与夜间GH分泌延长和清晨去甲肾上腺素水平升高有关。睡眠限制后胰岛素敏感性降低,胰岛素敏感性的降低与夜间NEFA水平的升高相关。
结论/解读:健康男性的睡眠限制会导致夜间和清晨NEFA水平升高,这可能部分导致了胰岛素抵抗以及与睡眠不足相关的糖尿病风险升高。