Genné-Bacon Elizabeth A, Trinko Joseph R, DiLeone Ralph J
Division of Molecular Psychiatry, Ribicoff Research Facilities, Department of Psychiatry, Yale University School of MedicineNew Haven, CT, USA; Department of Genetics, Yale University School of MedicineNew Haven, CT, USA.
Division of Molecular Psychiatry, Ribicoff Research Facilities, Department of Psychiatry, Yale University School of Medicine New Haven, CT, USA.
Front Behav Neurosci. 2016 Jul 4;10:132. doi: 10.3389/fnbeh.2016.00132. eCollection 2016.
Regulation of body weight is an important strategy for small prey animals to avoid capture. Field and laboratory studies have shown that prey animals reduce body size when subjected to long-term predator stimuli. However, the causes of predator-induced weight regulation are highly variable and the underlying mechanisms remain unclear. Understanding this phenomenon is important for gaining a better understanding of how animals regulate body weight under ethologically relevant conditions and has implications for obesity. Here we expose inbred C57BL/6J mice to a fear-inducing odorant (2,4,5-trimethylthiazole; mT) to model predation-induced weight regulation. Eight week-old mice were put on a 45% high fat diet (HFD) or chow diet (5% fat) and exposed daily to mT, an equally aversive dose of butyric acid (BA), or a neutral control scent (almond). mT-exposed mice in both diet groups gained significantly less weight over a 6-week period than BA-exposed mice. This differential weight gain appears unlikely to be due to differences in food intake and activity level, or brown adipose thermogenesis between the mT and BA groups. However, following chronic mT exposure we find increases in ΔFosB protein, a marker for long-term neural plasticity, in the dorsomedial hypothalamus (DMH)-an area previously implicated in chronic stress and defensive responses, as well as weight regulation. This study establishes a simplified and robust laboratory model of predation-mediated weight regulation with inbred lab mice and fear-inducing odor, and suggests a likely, yet undetermined, metabolic adaptation as contributing to this response.
体重调节是小型猎物动物避免被捕的一项重要策略。野外和实验室研究表明，猎物动物在受到长期捕食者刺激时会减小体型。然而，捕食者诱导的体重调节的原因高度可变，其潜在机制仍不清楚。了解这一现象对于更好地理解动物在行为学相关条件下如何调节体重以及对肥胖症具有重要意义。在这里，我们将近交系C57BL/6J小鼠暴露于一种诱发恐惧的气味剂（2,4,5-三甲基噻唑；mT）中，以模拟捕食诱导的体重调节。将8周龄的小鼠置于45%高脂肪饮食（HFD）或普通饮食（5%脂肪）中，并每天暴露于mT、同等厌恶剂量的丁酸（BA）或中性对照气味（杏仁）中。两个饮食组中暴露于mT的小鼠在6周内体重增加明显少于暴露于BA的小鼠。这种体重增加的差异似乎不太可能是由于mT组和BA组之间在食物摄入量、活动水平或棕色脂肪产热方面的差异。然而，在长期暴露于mT后，我们发现背内侧下丘脑（DMH）中ΔFosB蛋白增加，ΔFosB蛋白是长期神经可塑性的标志物，该区域先前与慢性应激、防御反应以及体重调节有关。本研究利用近交系实验小鼠和诱发恐惧的气味建立了一个简化且可靠的捕食介导的体重调节实验室模型，并表明一种可能但尚未确定的代谢适应是导致这种反应的原因。
