Sirohi Sunil, Van Cleef Arriel, Davis Jon F
Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, WA, United States; Laboratory of Endocrine and Neuropsychiatric Disorders, Division of Basic Pharmaceutical Sciences, College of Pharmacy, Xavier University of Louisiana, New Orleans, LA, United States.
Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, WA, United States.
Physiol Behav. 2017 Sep 1;178:187-195. doi: 10.1016/j.physbeh.2016.10.006. Epub 2016 Oct 17.
Binge eating and binge alcohol intake are behavioral manifestations of pathological feeding and alcohol use disorder (AUD), respectively. Binge-feeding and AUD have high comorbidity with other psychiatric disorders such as depression, which could have important implications for the management of these conditions. Importantly, these behaviors share many common features suggesting a singular etiology. However, the nature by which binge-feeding affects the development or maintenance of AUD is unclear. The present study examined the impact of a binge-feeding from a nutritionally complete high-fat diet (HFD) on initiation and maintenance of alcohol intake, anxiolytic behavior and central genetic changes in brain regions that control alcohol-reinforced behaviors. To do this, male Long-Evans rats received chow (controls) or HFD every three days (HFD-3D) or every day (HFD-ED) for 5weeks. Rodent chow and water were available ad-libitum to all groups throughout the experiment. Following 5weeks of HFD cycling, 20.0% ethanol or 2.0% sucrose intake was evaluated. In addition, anxiety-like behavior was measured using a light-dark box apparatus. Both HFD-3D and -ED groups of rats consumed significantly large amount of food during 2h HFD access sessions and reduced their chow intake in the next 22h. Surprisingly, binge-fed rats displayed attenuated acquisition of alcohol intake whereas sucrose consumption was unaffected. Rats exposed to HFD spent more time in the light side compared to chow controls, indicating that binge-feeding induced anxiolytic effects. In addition, alterations in the brain neurotensin system were observed following HFD exposure. These data indicate that binge-feeding behavior induces behavioral and genetic changes that help explain how alcohol intake is influenced by co-morbid eating disorders.
暴饮暴食和酗酒分别是病理性进食和酒精使用障碍(AUD)的行为表现。暴饮暴食和酒精使用障碍与其他精神疾病如抑郁症的共病率很高,这可能对这些疾病的管理具有重要意义。重要的是,这些行为具有许多共同特征,表明存在单一病因。然而,暴饮暴食影响酒精使用障碍发生或维持的本质尚不清楚。本研究考察了来自营养完整的高脂饮食(HFD)的暴饮暴食对酒精摄入的起始和维持、抗焦虑行为以及控制酒精强化行为的脑区的中枢基因变化的影响。为此,雄性Long-Evans大鼠每三天(HFD-3D)或每天(HFD-ED)接受普通饲料(对照组)或高脂饮食,持续5周。在整个实验过程中,所有组的啮齿动物均可自由获取普通饲料和水。在高脂饮食循环5周后,评估20.0%乙醇或2.0%蔗糖的摄入量。此外,使用明暗箱装置测量焦虑样行为。HFD-3D组和-ED组的大鼠在2小时的高脂饮食摄入期间均大量进食,并在接下来的22小时内减少了普通饲料的摄入量。令人惊讶的是,暴饮暴食的大鼠酒精摄入量的获得减弱,而蔗糖消耗量不受影响。与普通饲料对照组相比,暴露于高脂饮食的大鼠在亮侧停留的时间更长,这表明暴饮暴食诱导了抗焦虑作用。此外,在暴露于高脂饮食后观察到脑内神经降压素系统的改变。这些数据表明,暴饮暴食行为会引起行为和基因变化,这有助于解释共病的饮食失调如何影响酒精摄入。