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脱水-厌食症源于进食量减少,但不影响进食次数。

Dehydration-anorexia derives from a reduction in meal size, but not meal number.

机构信息

The Neuroscience Graduate Program, University of Southern California, Los Angeles, CA 90089-2520, United States.

出版信息

Physiol Behav. 2012 Jan 18;105(2):305-14. doi: 10.1016/j.physbeh.2011.08.005. Epub 2011 Aug 11.

Abstract

The anorexia that results from extended periods of cellular dehydration is an important physiological adaptation that limits the intake of osmolytes from food and helps maintain the integrity of fluid compartments. The ability to experimentally control both the development and reversal of anorexia, together with the understanding of underlying hormonal and neuropeptidergic signals, makes dehydration (DE)-anorexia a powerful model for exploring the interactions of neural networks that stimulate and inhibit food intake. However, it is not known which meal parameters are affected by cellular dehydration to generate anorexia. Here we use continuous and high temporal resolution recording of food and fluid intake, together with a drinking-explicit method of meal pattern analysis to explore which meal parameters are modified during DE-anorexia. We find that the most important factor responsible for DE-anorexia is the failure to maintain feeding behavior once a meal has started, rather than the ability to initiate a meal, which remains virtually intact. This outcome is consistent with increased sensitivity to satiation signals and post-prandial satiety mechanisms. We also find that DE-anorexia significantly disrupts the temporal distribution of meals across the day so that the number of nocturnal meals gradually decreases while diurnal meal number increases. Surprisingly, once DE-anorexia is reversed this temporal redistribution is maintained for at least 4 days after normal food intake has resumed, which may allow increased daily food intake even after normal satiety mechanisms are reinstated. Therefore, DE-anorexia apparently develops from a selective targeting of those neural networks that control meal termination, whereas meal initiation mechanisms remain viable.

摘要

长期细胞脱水导致的厌食症是一种重要的生理适应性反应,它限制了食物中渗透物的摄入,有助于维持体液隔室的完整性。能够实验性地控制厌食症的发展和逆转,以及对潜在激素和神经肽信号的理解,使得脱水(DE)-厌食症成为探索刺激和抑制进食的神经网络相互作用的有力模型。然而,目前尚不清楚哪些进餐参数会因细胞脱水而发生变化,从而导致厌食症。在这里,我们使用连续和高时间分辨率的食物和液体摄入记录,以及一种明确的饮水模式分析方法,来探讨在 DE-厌食症期间哪些进餐参数会发生变化。我们发现,导致 DE-厌食症的最重要因素是一旦开始进食,就无法维持进食行为,而进食的能力几乎完好无损。这一结果与增加对饱腹感信号和餐后饱腹感机制的敏感性一致。我们还发现,DE-厌食症会显著打乱一天中进餐的时间分布,导致夜间进餐次数逐渐减少,而白天进餐次数增加。令人惊讶的是,一旦 DE-厌食症得到逆转,这种时间重新分配至少会在恢复正常饮食后的 4 天内持续存在,这可能允许在恢复正常饱腹感机制后增加每日食物摄入量。因此,DE-厌食症显然是由于对控制进餐结束的神经网络的选择性靶向,而进餐启动机制仍然可行。

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