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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睡眠不足和高脂肪喂养对狗胰岛素敏感性和 β 细胞功能的影响。


目的/假设人们越来越认识到睡眠不足是肥胖和糖尿病发生的主要危险因素，临床研究中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损伤具有临床意义，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，尚未评估睡眠不足与高脂肪喂养对同一个体的相对影响。此外，据我们所知，不存在睡眠不足引起的代谢损伤的昼夜（白天活跃）非人类哺乳动物模型，这限制了我们研究睡眠与新陈代谢之间联系的能力。方法 这项研究在犬模型中进行 9 个月的高脂肪喂养之前和之后，通过 IVGTT 评估一晚完全睡眠不足对胰岛素敏感性和 β 细胞功能的影响。结果 瘦狗一晚完全睡眠不足对胰岛素敏感性的损害程度与长期高脂饮食 (HFD) 相似（正常睡眠：4.95 ± 0.45 mU-1 l-1 min-1；睡眠不足：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）。高胰岛素补偿是由慢性 HFD 引起的，表明 β 细胞对高脂肪喂养有足够的反应。相比之下，一晚睡眠不足后，β细胞没有出现代偿，这表明急性睡眠不足会导致代谢失调，如果在慢性睡眠不足期间持续存在这种情况，可能会增加患 2 型糖尿病的风险。 长期高脂肪喂养后，急性完全睡眠剥夺并未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提供了进一步的证据，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。