Energy homeostasis in leptin deficient Lepob/ob mice.
Energy homeostasis in leptin deficient Lepob/ob mice.
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DOI：
10.1371/journal.pone.0189784
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
LeDuc CA
中科院分区：
文献类型：
--
作者：
Skowronski AA;Ravussin Y;Leibel RL;LeDuc CA
在小鼠和人类中，维持体重减轻与每单位代谢质量的能量消耗减少和饥饿感增加有关。由于脂肪量减少，循环瘦素浓度降低，为这种反应提供了一个主要信号。然而，瘦素缺乏（Lepob/ob）小鼠（和瘦素受体缺乏的Zucker大鼠）通过非瘦素依赖机制减少体重减轻后的能量消耗。为了确定这些机制，Lepob/ob小鼠被随意喂养（AL组，n = 21）或限制为每天3千卡的食物（CR组，n = 21）。在减少初始体重的20%后（大约2周），CR小鼠通过滴定再喂食将初始体重的80%稳定在两周，然后从食物限制中释放。CR小鼠保存了能量（白天比根据体重和组成预测的低17%，晚上比预测的低52%）；并且，当释放到自由喂养时，CR小鼠在5周内恢复了脂肪和瘦体重（到AL水平）。CR小鼠这样做时，它们的随意热量摄入与AL动物相同。在热量限制的情况下，CR小鼠的呼吸交换率（RER = 0.89）显著低于AL小鼠（0.94）；放归自由饲养后，RER（1.03）显著高于AL组（0.93），与它们的合成代谢状态一致。这些结果证实，在先天性瘦素缺乏的动物中，瘦素不是伴随体重减轻的能量消耗代偿性减少所必需的，但表明体重减轻状态的贪食是瘦素依赖的。
Maintenance of reduced body weight is associated both with reduced energy expenditure per unit metabolic mass and increased hunger in mice and humans. Lowered circulating leptin concentration, due to decreased fat mass, provides a primary signal for this response. However, leptin deficient (Lepob/ob) mice (and leptin receptor deficient Zucker rats) reduce energy expenditure following weight reduction by a necessarily non-leptin dependent mechanisms. To identify these mechanisms, Lepob/ob mice were fed ad libitum (AL group; n = 21) or restricted to 3 kilocalories of chow per day (CR group, n = 21). After losing 20% of initial weight (in approximately 2 weeks), the CR mice were stabilized at 80% of initial body weight for two weeks by titrated refeeding, and then released from food restriction. CR mice conserved energy (-17% below predicted based on body mass and composition during the day; -52% at night); and, when released to ad libitum feeding, CR mice regained fat and lean mass (to AL levels) within 5 weeks. CR mice did so while their ad libitum caloric intake was equal to that of the AL animals. While calorically restricted, the CR mice had a significantly lower respiratory exchange ratio (RER = 0.89) compared to AL (0.94); after release to ad libitum feeding, RER was significantly higher (1.03) than in the AL group (0.93), consistent with their anabolic state. These results confirm that, in congenitally leptin deficient animals, leptin is not required for compensatory reduction in energy expenditure accompanying weight loss, but suggest that the hyperphagia of the weight-reduced state is leptin-dependent.
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影响因子：
4.1
作者：
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