不少人逢年过节容易暴饮暴食，有时感觉饱了仍然不停地进食。美国研究人员指出，这些人之所以停不下嘴，可能是一种激素在“作怪”。这一结果刊载于《生物精神病学》杂志网站。
美国得克萨斯大学西南医学中心研究人员通过实验发现，一种名为“饥饿激素”的胃肽令小鼠在不饿的情况下找食吃。研究人员为小鼠搭了两间小屋，其中一间条纹墙面的小屋内放有高热量美味食物，另一间灰色墙面的小屋里则放有低热量食物。经过多次训练后，小鼠记住哪间小屋里放的是什么东西。接着，研究人员喂饱小鼠后让它们选择进一间小屋。结果发现，注射了“饥饿激素”的小鼠更倾向于进入条纹墙面的小屋，即便其中并没有食物。但未注射“饥饿激素”的小鼠没有表现出倾向性。研究负责人之一杰弗里齐格曼副教授的话报道：“我们的研究表明，这种激素会影响与进食有关的行为，进而导致过量饮食。”
齐格曼认为，“饥饿激素”可能令人对食物产生格外的“好感”。他解释说：“小鼠的行为与吃东西无关，只是为了获得更多快感。”这项研究的另一名负责人、内科学博士后研究生马里奥佩雷洛说：“我们认为，‘饥饿激素’令小鼠去寻觅高热量食物，因为它们记得它有多美味。”“即使小屋内没有食物也没关系，小鼠仍认为它与某种能引起快感的事物存在关联，”他说。人类和小鼠在脑细胞联结、激素类型和大脑“快感中枢”方面有相同点。实验中小鼠的行为与其他研究成瘾性实验中动物寻求快感的行为一样。
然而，“饥饿激素”并非令人不停吃东西的唯一原因。其他一些因素也会导致人们过量饮食。首先是基因影响。英国帝国理工学院研究人员2003年发现，一种名为“GAD2”的基因容易导致肥胖。这种基因会加速大脑中一种神经递质的合成，进而刺激人们进食。其次是多巴胺水平。《行为神经学》杂志2007年刊登研究报告指出，体内多巴胺水平较低的人更有可能为寻求快感而暴饮暴食。还有心理原因。一个常见现象是不少失意的人会大吃特吃。最后是习惯问题。如果你喜欢一边看电影一边吃甜点，那么在看大片《阿凡达》时，你也可能带上一桶爆米花，虽然你并不饿。
推荐原始出处：
Biological Psychiatry doi:10.1016/j.biopsych.2009.10.030
Ghrelin Increases the Rewarding Value of High-Fat Diet in an Orexin-Dependent Manner
Mario Perelloa, Ichiro Sakataa, Shari Birnbaumb, Jen-Chieh Chuanga, Sherri Osborne-Lawrencea, Sherry A. Rovinskya, Jakub Woloszyna, Masashi Yanagisawac, Michael Lutterb and Jeffrey M. Zigmana, b, ,
a Department of Internal Medicine (Divisions of Hypothalamic Research and Endocrinology " Metabolism), The University of Texas Southwestern Medical Center, Dallas, Texas
b Department of Psychiatry, The University of Texas Southwestern Medical Center, Dallas, Texas
c Department of Molecular Genetics and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center, Dallas, Texas
Background
Ghrelin is a potent orexigenic hormone that likely impacts eating via several mechanisms. Here, we hypothesized that ghrelin can regulate extra homeostatic, hedonic aspects of eating behavior.
Methods
In the current study, we assessed the effects of different pharmacological, physiological, and genetic models of increased ghrelin and/or ghrelin-signaling blockade on two classic behavioral tests of reward behavior: conditioned place preference (CPP) and operant conditioning.
Results
Using both CPP and operant conditioning, we found that ghrelin enhanced the rewarding value of high-fat diet (HFD) when administered to ad lib-fed mice. Conversely, wild-type mice treated with ghrelin receptor antagonist and ghrelin receptor-null mice both failed to show CPP to HFD normally observed under calorie restriction. Interestingly, neither pharmacologic nor genetic blockade of ghrelin signaling inhibited the body weight homeostasis-related, compensatory hyperphagia associated with chronic calorie restriction. Also, ghrelin's effects on HFD reward were blocked in orexin-deficient mice and wild-type mice treated with an orexin 1 receptor antagonist.
Conclusions
Our results demonstrate an obligatory role for ghrelin in certain rewarding aspects of eating that is separate from eating associated with body weight homeostasis and that requires the presence of intact orexin signaling.
