AIMS/HYPOTHESIS Insufficient sleep is increasingly recognised as a major risk factor for the development of obesity and diabetes, and short-term sleep loss in clinical studies leads to a reduction in insulin sensitivity. Sleep loss-induced metabolic impairments are clinically relevant, since reductions in insulin sensitivity after sleep loss are comparable to insulin sensitivity differences between healthy individuals and those with impaired glucose tolerance. However, the relative effects of sleep loss vs high-fat feeding in the same individual have not been assessed. In addition, to our knowledge no diurnal (active during the daytime) non-human mammalian model of sleep loss-induced metabolic impairment exists, which limits our ability to study links between sleep and metabolism. METHODS This study examined the effects of one night of total sleep deprivation on insulin sensitivity and beta cell function, as assessed by an IVGTT, before and after 9 months of high-fat feeding in a canine model. RESULTS One night of total sleep deprivation in lean dogs impaired insulin sensitivity to a similar degree as a chronic high-fat diet (HFD)(normal sleep: 4.95 ± 0.45 mU-1 l-1 min-1; sleep deprivation: 3.14 ± 0.21 mU-1 l-1 min-1; HFD: 3.74 ± 0.48 mU-1 l-1 min-1; mean ± SEM). Hyperinsulinaemic compensation was induced by the chronic HFD, suggesting adequate beta cell response to high-fat feeding. In contrast, there was no beta cell compensation after one night of sleep deprivation, suggesting that there was metabolic dysregulation with acute sleep loss that, if sustained during chronic sleep loss, could contribute to the risk of type 2 diabetes. After chronic high-fat feeding, acute total sleep deprivation did not cause further impairments in insulin sensitivity (sleep deprivation + chronic HFD: 3.28 mU-1 l-1 min-1). CONCLUSIONS/INTERPRETATION Our findings provide further evidence that sleep is important for metabolic health and establish a diurnal animal model of metabolic disruption during insufficient sleep.

中文翻译：

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睡眠剥夺和高脂肪喂养对狗的胰岛素敏感性和β细胞功能的影响。

目标/假设 睡眠不足越来越被认为是肥胖和糖尿病发展的主要风险因素，临床研究中的短期睡眠不足会导致胰岛素敏感性降低。睡眠不足引起的代谢障碍在临床上是相关的，因为睡眠不足后胰岛素敏感性的降低与健康个体和糖耐量受损者之间的胰岛素敏感性差异相当。然而，尚未评估同一个体中睡眠不足与高脂肪喂养的相对影响。此外，据我们所知，不存在昼夜（白天活跃）非人类哺乳动物睡眠不足引起的代谢障碍模型，这限制了我们研究睡眠与新陈代谢之间联系的能力。方法 本研究通过 IVGTT 评估，在犬模型中高脂喂养 9 个月之前和之后，检查一晚完全睡眠剥夺对胰岛素敏感性和 β 细胞功能的影响。结果 瘦狗一晚完全睡眠剥夺会损害胰岛素敏感性，其程度与慢性高脂饮食 (HFD) 相似（正常睡眠：4.95 ± 0.45 mU-1 l-1 min-1；睡眠剥夺：3.14 ± 0.21 mU-1 l-1 min-1；HFD：3.74 ± 0.48 mU-1 l-1 min-1；平均值 ± SEM）。慢性HFD诱导高胰岛素代偿，表明β细胞对高脂肪喂养有足够的反应。相比之下，一晚睡眠剥夺后没有β细胞代偿，这表明急性睡眠丧失存在代谢失调，如果在慢性睡眠丧失期间持续存在，可能会增加患 2 型糖尿病的风险。长期高脂喂养后，急性完全睡眠剥夺不会导致胰岛素敏感性进一步受损（睡眠剥夺 + 慢性 HFD：3.28 mU-1 l-1 min-1）。结论/解释 我们的研究结果进一步证明睡眠对代谢健康很重要，并建立了睡眠不足期间代谢紊乱的昼夜动物模型。