Schmid Sebastian M, Hallschmid Manfred, Jauch-Chara Kamila, Bandorf Nadine, Born Jan, Schultes Bernd
Department of Internal Medicine, University of Luebeck, Germany.
J Clin Endocrinol Metab. 2007 Aug;92(8):3044-51. doi: 10.1210/jc.2006-2788. Epub 2007 May 22.
Sleep loss has immediate effects on metabolic function that in the long run may contribute to the development of obesity and type 2 diabetes.
Our objective was to explore the neuroendocrine mechanisms mediating the acute effects of sleep deprivation on blood glucose regulation under basal and hypoglycemic conditions.
In a randomized, crossover study in 10 healthy young men, plasma concentrations of relevant hormones were examined during basal rest, a subsequent stepwise hypoglycemic clamp after one night of total sleep deprivation (SD) and one night of regular sleep.
Basal glucagon concentrations were decreased (P = 0.022) and C-peptide levels were slightly reduced after SD (P = 0.085), compared with regular sleep. During hypoglycemia after SD, the glucagon increase relative to baseline was enhanced (P = 0.034) and the relative decrease in C-peptide was reduced (P = 0.013). Also, the relative increase in norepinephrine was reduced (P = 0.031). SD did not affect epinephrine, ACTH, cortisol, lactate, beta-hydroxybutyrate, or nonesterified fatty acids during hypoglycemia, but overall, plasma nonesterified fatty acid levels were reduced after SD (P = 0.009). SD markedly increased rated hunger during basal rest (P < 0.008), resulting in a dampened relative increase during hypoglycemia (P < 0.009). Unexpectedly, despite distinct alterations in basal secretory activity, the absolute amplitude of hormonal counterregulation and hunger responses to hypoglycemia was not affected by SD.
Short-term SD distinctly alters hormonal glucose regulation, affecting especially pancreatic islet secretion, and also increases hunger. Immediate perturbations in the dynamic regulation of energy metabolism caused by acute sleep curtailment may contribute to the association between chronic sleep loss and metabolic disorders.
睡眠不足对代谢功能有直接影响，从长远来看，可能会导致肥胖和2型糖尿病的发生。
我们的目的是探讨在基础和低血糖条件下介导睡眠剥夺对血糖调节急性影响的神经内分泌机制。
在一项针对10名健康年轻男性的随机交叉研究中，在基础休息期间、一夜完全睡眠剥夺（SD）和一夜正常睡眠后的后续逐步低血糖钳夹期间，检测相关激素的血浆浓度。
与正常睡眠相比，SD后基础胰高血糖素浓度降低（P = 0.022），C肽水平略有降低（P = 0.085）。在SD后的低血糖期间，相对于基线的胰高血糖素增加增强（P = 0.034），C肽的相对降低减少（P = 0.013）。此外，去甲肾上腺素的相对增加减少（P = 0.031）。SD在低血糖期间不影响肾上腺素、促肾上腺皮质激素、皮质醇、乳酸、β-羟基丁酸或非酯化脂肪酸，但总体而言，SD后血浆非酯化脂肪酸水平降低（P = 0.009）。SD在基础休息期间显著增加饥饿评分（P < 0.008），导致低血糖期间相对增加减弱（P < 0.009）。出乎意料的是，尽管基础分泌活动有明显改变，但激素对抗调节的绝对幅度和对低血糖的饥饿反应不受SD影响。
短期SD明显改变激素对葡萄糖的调节，尤其影响胰岛分泌，还会增加饥饿感。急性睡眠减少引起的能量代谢动态调节的即时扰动可能导致慢性睡眠不足与代谢紊乱之间的关联。
