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高脂维持饮食减弱后脑神经元对胆囊收缩素的反应。

High fat maintenance diet attenuates hindbrain neuronal response to CCK.

作者信息

Covasa M, Grahn J, Ritter R C

机构信息

Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, Washington 99164, USA.

出版信息

Regul Pept. 2000 Jan 29;86(1-3):83-8. doi: 10.1016/s0167-0115(99)00084-1.

DOI:10.1016/s0167-0115(99)00084-1
PMID:10672906
Abstract

Rats maintained on a high fat diet reduce their food intake less in response to exogenous cholecystokinin (CCK) than rats maintained on a low fat diet. In addition, inhibition of gastric emptying by CCK is markedly attenuated in rats maintained on a high fat diet. Both inhibition of food intake and gastric emptying by CCK are mediated by sensory fibers in the vagus nerve. These fibers terminate on dorsal hindbrain neurons of the nucleus of the solitary tract and area postrema. To determine whether diet-induced changes in the control of feeding and gastric emptying are accompanied by altered vagal sensory responsiveness, we examined dorsal hindbrain expression of Fos-like immunoreactivity (Fos-li) following intraperitoneal CCK injection of rats maintained on high fat or low fat diets. Following CCK, there were numerous Fos-li nuclei in the area postrema and in the commissural and medial subnuclei of the nucleus of the solitary tract of rats maintained on a low fat diet. However, Fos-li was absent or rare in the brains of rats maintained on a high fat diet. These data suggest that the vagal sensory response to exogenous CCK is reduced in rats maintained on a high fat diet. Our results also are consistent with our previous findings that CCK-induced reduction of food intake and gastric emptying are both attenuated in rats maintained on a high fat diet. In addition our results support the hypothesis that attenuation of CCK-induced inhibition of food intake and gastric emptying may be due to diet-induced diminution of vagal CCK responsiveness.

摘要

与食用低脂饮食的大鼠相比,食用高脂饮食的大鼠对外源性胆囊收缩素(CCK)的反应导致食物摄入量减少得更少。此外,CCK对食用高脂饮食大鼠的胃排空抑制作用明显减弱。CCK对食物摄入和胃排空的抑制作用均由迷走神经中的感觉纤维介导。这些纤维终止于孤束核和最后区的背侧后脑神经元。为了确定饮食诱导的进食和胃排空控制变化是否伴随着迷走神经感觉反应性的改变,我们检查了腹腔注射CCK后,食用高脂或低脂饮食大鼠的后脑背侧Fos样免疫反应性(Fos-li)的表达。注射CCK后,食用低脂饮食大鼠的最后区以及孤束核的连合和内侧亚核中有许多Fos-li阳性细胞核。然而,在食用高脂饮食大鼠的大脑中,Fos-li不存在或很少见。这些数据表明,食用高脂饮食的大鼠对外源性CCK的迷走神经感觉反应降低。我们的结果也与我们之前的发现一致,即CCK诱导的食物摄入量和胃排空减少在食用高脂饮食的大鼠中均减弱。此外,我们的结果支持这样的假设,即CCK诱导的食物摄入和胃排空抑制作用减弱可能是由于饮食诱导的迷走神经对CCK反应性降低所致。

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