Greenberg D, Smith G P
Department of Psychiatry, Cornell University Medical College, White Plains, New York 10605, USA.
Psychosom Med. 1996 Nov-Dec;58(6):559-69. doi: 10.1097/00006842-199611000-00004.
To present evidence on the control of the size of fatty meals in the context of the result of interactions of orosensory positive-feedback and postingestive negative-feedback mechanisms activated by fat stimuli in rodent models of feeding and of obesity.
We examined the effects of orosensory stimuli and postingestive stimuli in Sprague-Dawley rats, and in the genetically obese Zucker (fa/fa) rat. We used the sham feeding rat preparation to isolate the orosensory stimulating and postingestive satiating properties of oils. The negative-feedback satiating properties of fats were elicited by intestinal infusions of fats. The Zucker rat is an animal model of obesity with abnormal control of meal size and increased intake of fats. Using this model we further examined the interaction of orosensory and postingestive stimuli in the control of meal size.
The orosensory properties of fats are sufficient to drive sham feeding and are not dependent on the postabsorptive metabolic consequences of oils in normal and Zucker rats. The satiating action of fats must act at preabsorptive sites because reduction of intake occurs before absorption of fat. The satiating potency of fats is dependent upon their specific chemical conformation and is mediated by endogenous cholecystokinin and afferent fibers of the abdominal vagus. We have found that oils produce significantly more orosensory positive feedback in obese Zucker rats than in lean rats in experimental tests of preference. This is probably the major abnormal mechanism responsible for the increased preference for fats that is characteristic of obese rats because we have not identified any significant decrease in the postingestive satiating potency of fats in obese Zucker rats.
Fat intake is controlled by both orosensory and postingestive stimuli in normal and genetically obese rodents. In the Zucker rat the investigation of this model of genetic obesity has produced data that is congruent with the preference for high fat foods in obese people and suggests further experiments directed toward a deeper understanding of the controls of fat intake and how they are disordered.
在啮齿动物摄食和肥胖模型中，根据脂肪刺激激活的口咽部正反馈和摄食后负反馈机制相互作用的结果，提供关于控制高脂餐食量的证据。
我们研究了口咽部刺激和摄食后刺激对Sprague-Dawley大鼠以及遗传性肥胖的Zucker（fa/fa）大鼠的影响。我们采用假饲大鼠制备方法来分离油的口咽部刺激和摄食后饱腹感特性。通过肠道输注脂肪来引发脂肪的负反馈饱腹感特性。Zucker大鼠是一种肥胖动物模型，其食量控制异常且脂肪摄入量增加。利用该模型，我们进一步研究了口咽部和摄食后刺激在食量控制中的相互作用。
在正常和Zucker大鼠中，脂肪的口咽部特性足以驱动假饲，且不依赖于油的吸收后代谢后果。脂肪的饱腹感作用必须在吸收前部位起作用，因为在脂肪吸收之前摄入量就已减少。脂肪的饱腹感效力取决于其特定的化学构象，并由内源性胆囊收缩素和腹腔迷走神经的传入纤维介导。我们发现在偏好实验测试中，与瘦大鼠相比，肥胖的Zucker大鼠对油产生的口咽部正反馈明显更多。这可能是肥胖大鼠对脂肪偏好增加的主要异常机制，因为我们未发现肥胖的Zucker大鼠中脂肪的摄食后饱腹感效力有任何显著降低。
在正常和遗传性肥胖的啮齿动物中，脂肪摄入量受口咽部和摄食后刺激的控制。在Zucker大鼠中，对这种遗传性肥胖模型的研究得出的数据与肥胖人群对高脂肪食物的偏好一致，并提示进一步开展实验，以更深入地了解脂肪摄入的控制机制以及这些机制是如何紊乱的。
