Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901, USA.
Physiol Behav. 2012 Feb 1;105(3):720-6. doi: 10.1016/j.physbeh.2011.09.021. Epub 2011 Oct 6.
Endogenous cannabinoid signaling, mediated predominately by CB1 receptor activation, is involved in food intake control and body weight regulation. Despite advances in determining the role of the CB1 receptor in obesity, its involvement in the driven nature of eating pathologies has received little attention. The present study examined CB1 receptor alterations as a consequence of dietary-induced binge eating in female Sprague Dawley rats. Four control groups were used to control for calorie restriction and highly palatable food variables characterizing this behavioral model. All groups were kept on their respective feeding schedules for 6-weeks and were given a uniform 33% calorie restriction (~22 h food deprivation) prior to sacrifice. Our findings indicate that regional CB1 mRNA and density were influenced by dietary conditions, but were not specific to the dietary-induced binge eating paradigm used. An increase of approximately 50% (compared with naive controls) in CB1 receptor mRNA levels in the nucleus of the solitary tract as measured by in situ hybridization was found in animals receiving continuous access to a highly palatable food (i.e., vegetable shortening with 10% sucrose). This group also had a significant increase in body weight and adiposity. An approximate 20% reduction in CB1 mRNA was observed in the cingulate cortex (areas 1 and 2) in animals exposed to an intermittent schedule of feeding, compared with groups that had ad libitum feeding schedules (i.e., continuous access and naive controls). Receptor density as measured by [(3)H]CP55,940 autoradiography, was reduced by approximately 30% in the nucleus accumbens shell region in groups receiving repeated access to the highly palatable food. Taken together, these findings indicate that dietary conditions can differentially influence CB1 receptors in forebrain and hindbrain regions.
内源性大麻素信号转导主要通过 CB1 受体的激活来介导，参与了食物摄入控制和体重调节。尽管在确定 CB1 受体在肥胖中的作用方面已经取得了进展，但它在进食病理驱动性质中的作用却很少受到关注。本研究检查了饮食诱导的暴食行为对雌性 Sprague Dawley 大鼠 CB1 受体改变的影响。使用了四个对照组来控制该行为模型的特征，即热量限制和高美味食物变量。所有组都按照各自的喂养时间表喂养 6 周，并在牺牲前接受了统一的 33%热量限制（~22 小时禁食）。我们的研究结果表明，区域 CB1 mRNA 和密度受到饮食条件的影响，但与使用的饮食诱导暴食行为范式无关。通过原位杂交测量，在连续接受高美味食物（即 10%蔗糖的蔬菜起酥油）的动物的孤束核中，CB1 受体 mRNA 水平增加了约 50%（与对照相比）。该组的体重和肥胖程度也显著增加。与自由喂养组（即连续接触和对照）相比，暴露于间歇性进食方案的动物的扣带皮层（区域 1 和 2）中 CB1 mRNA 减少了约 20%。通过 [(3)H]CP55,940 放射自显影测量，在反复接触高美味食物的动物的伏隔核壳区，受体密度降低了约 30%。综上所述，这些发现表明，饮食条件可以在大脑前区和后脑区对 CB1 受体产生不同的影响。
