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目的:探讨给予间歇性摄食大鼠模型(Intermittent Access Model[IAM])果糖是否可使IAM大鼠对果糖产生暴食行为,以及下丘脑外侧核(LHA)和伏隔核Orexin(ORX)神经元对果糖暴食行为的影响。方法:给予IAM大鼠4%、8%或12%的果糖溶液及生理盐水,观察和记录大鼠果糖摄入量及能否产生果糖暴食行为;测定果糖凝集反应大鼠伏隔核壳(NAc shell)、伏隔核核(NAc core)和背侧纹状体(Dorsal striatum)多巴胺受体(D1R、D2R)数目(Bmax)和受体亲和力(Kd);分别监测长期和短期IAM大鼠室旁核(PVN)、杏仁核(CeA)、伏隔核(NAc)等相关核团的C-Fos神经元活性(Fos-IR);给予长期IAM大鼠OX1R拮抗剂SB334867,记录大鼠摄食量。结果:长期IAM大鼠表现出果糖暴食行为,但相应的多巴胺受体数目并未改变。与对照组相比,果糖暴食组大鼠伏隔核c-Fos蛋白减少,神经元活性降低。短期IAM大鼠可产生果糖暴食但Fos-IR未改变。给予长期IAM大鼠OX1R拮抗剂SB-334867(30 mg/kg),大鼠果糖暴食量和食物摄入量均减少。结论:长短期IAM大鼠均可产生果糖暴食行为;仅长期果糖暴食可致Orexin释放增加,减少伏隔核Orexin神经元激活,增强外侧核Orexin神经元激活。
OBJECTIVE: To investigate whether the administration of fructose to Intermittent Access Model (IAM) can induce binge eating behavior of fructose in IAM rats, and the effect of Orexin (ORX) neurons in hypothalamic lateral (LHA) and nucleus accumbens Effects of fructose binge eating behavior. Methods: 4%, 8% or 12% fructose solution and saline were given to IAM rats. The fructose intake and fructose binge eating behavior of rats were observed and recorded. The expression of NAc shell, nucleus accumbens nucleus (NAc core) and dorsal striatum dopamine receptors (D2R) number (Bmax) and receptor affinity (Kd); long term and short term IAM rat ventricular C-Fos neuron activity (Fos-IR) of related nucleus such as PVN, CeA, NAc and the like. The long-term Iox rat OX1R antagonist SB334867 was administered to rats. . RESULTS: Long-term IAM rats exhibited fructose binge behavior but the corresponding numbers of dopamine receptors did not change. Compared with the control group, fructose diet group rats nucleus accumbens c-Fos protein decreased, decreased neuronal activity. Short-term IAM rats produce fructose overeating but Fos-IR is unchanged. Administration of OX1R antagonist SB-334867 (30 mg / kg) to long-term IAM rats resulted in reduced fructose overdose and food intake. CONCLUSION: Overexpression of Orexin can be induced by long-term fructose overeating in both long and short-term IAM rats. Orexin neuron activation in nucleus accumbens nucleus and Orexin neuron activation in the lateral nucleus are enhanced.