Department of Psychological Sciences and Ingestive Behavior Research Center, Purdue University, West Lafayette, IN 47907, USA.
Physiol Behav. 2012 Feb 28;105(4):975-81. doi: 10.1016/j.physbeh.2011.11.006. Epub 2011 Nov 15.
The consumption of a large food bolus leads to stomach distension. Gastric distension potently signals the termination of a meal by stimulating gastric mechanoreceptors and activating neuroendocrine circuitry. The ability to terminate a meal is altered in disorders such as bulimia nervosa (BN), binge-eating disorder (BED) and certain subtypes of obesity in which large quantities of food are frequently ingested. When a large meal is consumed, the stomach is rapidly stretched. We modeled this rapid distension of the stomach in order to determine if the neuroendocrine abnormalities present in these disorders, including increased gastric capacit3y, leptin dysregulation, and alterations in neuropeptide Y (NPY), and proopiomelanocortin (POMC) expression, were influenced by the rapid stretch aspect of repeatedly consuming a large meal. To test the effects of repeated gastric distension (RGD) on neuroendocrine factors involved in energy homeostasis, a permanent intra-gastric balloon was implanted in rats, and briefly inflated daily for 4 weeks. Though body weights and daily food intakes remained equivalent in RGD and control rats, a significant delay in the onset of feeding was present during the first and second, but not the third and fourth weeks of inflations. Despite equivalent body weights and daily caloric consumption, RGD animals had significantly decreased leptin levels (p<0.05), and tended to have increased fasting arcuate NPY levels (p=0.08), which were suppressed more than control animals following food intake (control and RGD decreases from baseline were 184.95% and 257.42%, respectively). NPY expression in the nucleus of the solitary tract followed a similar pattern. These data demonstrate that the act of regularly distending the stomach can have effects on the regulation of energy balance that are independent from those related to caloric consumption, and may be related to disorders such as BN, BED, and certain types of obesity in which meal termination is impaired.
大量食物摄入会导致胃胀。胃胀通过刺激胃机械感受器和激活神经内分泌回路，有力地发出进食终止的信号。在神经性贪食症（BN）、暴食障碍（BED）和某些肥胖亚型等疾病中，进食行为会发生改变，这些疾病中大量食物经常被摄入。当摄入大量食物时，胃会迅速扩张。我们模拟了胃的这种快速扩张，以确定这些疾病中存在的神经内分泌异常是否受到反复摄入大量食物的快速扩张方面的影响，这些异常包括胃容量增加、瘦素失调以及神经肽 Y（NPY）和前阿黑皮素原（POMC）表达的改变。为了测试反复胃扩张（RGD）对参与能量稳态的神经内分泌因子的影响，在大鼠中植入了永久性胃内气球，并在 4 周内每天短暂充气。尽管 RGD 组和对照组大鼠的体重和每日食物摄入量保持相等，但在充气的第一和第二周，而不是第三和第四周，进食开始出现明显延迟。尽管体重和每日热量摄入相等，RGD 动物的瘦素水平显著降低（p<0.05），并且空腹弓状核 NPY 水平升高的趋势（p=0.08），与对照组动物相比，进食后抑制更为明显（对照组和 RGD 从基线的降低分别为 184.95%和 257.42%）。孤束核中的 NPY 表达也呈现出类似的模式。这些数据表明，定期扩张胃的行为会对能量平衡的调节产生影响，这些影响独立于与热量摄入相关的影响，并且可能与 BN、BED 和某些肥胖类型等疾病有关，这些疾病中进食终止受损。
