近年来，由于无节制摄入高热量饮食，超重/肥胖已成为我国非常严重的公共卫生问题。本领域的相关工作多集中于对能量代谢和进食行为的内稳调控机制进行研究，而对食物奖赏的过度寻求以及由此而来的强迫进食等摄食障碍则关注较少。强迫进食很有可能与目前高热量的膳食结构相关：高热量食物可能通过影响中枢奖赏系统诱发强迫进食，但涉及的脑区和具体机制我们知之甚少。我们的预实验发现，高脂食物喂养一周就足以诱发小鼠的强迫进食行为，提示强迫性进食可能是高脂食物诱发肥胖的行为机制之一。我们的c-Fos染色结果表明，强迫进食小鼠的丘脑室旁核（PVT）被过度激活，提示高脂食物诱发的强迫进食与PVT的活动密切相关。我们将以高脂食物诱发的强迫进食小鼠为模型，采用行为学、电生理、免疫组化及光遗传学/药理遗传学等实验技术，研究PVT及其相关核团-主要是下丘脑腹内侧核-在强迫进食中的作用，为肥胖的防治提供新的、基于中枢的理论和应用依据。

Since the last two decades, overweight/obesity has become a serious public health problem in China. The availability of high-calorie food is a major factor contributing to this obesity epidemic. In this field, the mechanisms relating to the disturbed homeostatic regulation of food intake have been well understood. However, the mechanisms underlying increased motivation to consume food, particularly the compulsive eating behavior, are still unclear.We have shown that 1-week high-fat diet consumption is sufficient to induce compulsive eating behavior in mice, suggesting that compulsive eating may contribute to high-fat diet-induced obesity. Importantly, high-fat diet-induced compulsive eating caused a high level of c-Fos activation in the paraventricular nucleus of the thalamus (PVT) in mice. In this project, we will use a combination of behavioral, electrophysiology, immunohistochemistry, and optogenetics/pharmacogenetics methods, to explore the central role of PVT, along with its inputs and outputs, in high-fat diet-induced compulsive eating, to provide a new insight into the pathogenesis of obesity.