Late dinner impairs glucose tolerance in MTNR1B risk allele carriers: A randomized, cross-over study.

Late dinner impairs glucose tolerance in MTNR1B risk allele carriers: A randomized, cross-over study.
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DOI:
10.1016/j.clnu.2017.04.003
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发表时间:
2018-08
期刊:
Clinical nutrition (Edinburgh, Scotland)
影响因子:
--
通讯作者:
Garaulet M
Garaulet M
中科院分区:
其他
文献类型:
--
作者:
Lopez-Minguez J;Saxena R;Bandín C;Scheer FA;Garaulet M

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深夜晚餐进食与2型糖尿病风险增加有关。潜在的机制尚不清楚。一个解释性假设是,循环褪黑激素升高和高葡萄糖浓度(表征晚吃)的同时发生导致葡萄糖耐量受损。然而,迄今为止还没有研究测试生理褪黑激素浓度对葡萄糖耐受性的影响。褪黑激素受体MTNR1B作为糖尿病风险基因的发现为褪黑激素的生理水平在葡萄糖控制中的作用提供了证据。本研究的目的是验证内源性褪黑激素在晚吃饭时影响血糖控制的假设。注册于ClinicalTrials.gov标识号NCT 03003936我们进行了一项随机交叉试验,以比较存在(晚餐后)或不存在(晚餐前)生理褪黑激素的葡萄糖耐受性,并比较了MTNR 1B风险等位基因纯合子携带者和非携带者之间的结果。同时进餐时间与内源性褪黑激素浓度升高导致葡萄糖耐量受损。这种影响在MTNR1B风险携带者中比在非携带者中更强。此外,晚吃只会显著损害高危携带者的葡萄糖耐量,而非高危携带者。晚餐时间与MTNR1B的相互作用支持内源性褪黑激素在葡萄糖耐量受损中的因果作用。这些结果表明,将晚餐时间提前可能会导致更好的葡萄糖耐受性,特别是在MTNR1B携带者中。
Late-night-dinner eating is associated with increased risk for type-2-diabetes. The underlying mechanism is unclear. One explanatory hypothesis is that the concurrence of elevated circulating melatonin and high glucose concentrations (characterizing late-eating) leads to impaired glucose-tolerance. However, to date no study has tested the influence of physiological melatonin concentrations on glucose-tolerance. The discovery of melatonin receptor MTNR1B as a diabetes risk gene provides evidence for a role of physiological levels of melatonin in glucose control. The aim of our study was to test the hypothesis that endogenous melatonin worsens glucose control when eating-late. Registered under ClinicalTrials.gov Identifier no. NCT03003936 We performed a randomized, cross-over trial to compare glucose-tolerance in the presence (late-dinner) or absence (early-dinner) of physiological melatonin and we compared the results between homozygous carriers and non-carriers of the MTNR1B risk allele. The concurrence of meal timing with elevated endogenous melatonin concentrations resulted in impaired glucose-tolerance. This effect was stronger in MTNR1B risk-carriers than in non-carriers. Furthermore, eating-late significantly impaired glucose tolerance only in risk-carriers and not in the non-risk carriers. The interaction of dinner timing with MTNR1B supports a causal role of endogenous melatonin in the impairment of glucose-tolerance. These results suggest that moving the dinner to an earlier time may result in better glucose-tolerance specially in MTNR1B carriers.
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发表时间: 2016-05
期刊: Trends in endocrinology and metabolism: TEM
影响因子: --
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