Drivers of eating behaviour during chronic overconsumption: Role of food hedonics (liking & wanting) and peptide biomarkers on satiation and satiety.

该项目将调查在长期过度消费（过量摄入卡路里）期间发生的饮食行为的驱动因素。过度消费是重要的一个主要原因，体重（再）增加和肥胖。据说许多发达国家存在的社会类型代表了“服从”环境。这种类型的环境促进了食物的高消费（以及鼓励久坐），并产生快速体重增加，导致肥胖。肥胖环境为人们提供了暴饮暴食的可能性。人们能够吃太多的一些食物，因为过度激活享乐（快乐相关）过程，或因为在稳态过程的缺陷。首先，这意味着人们会吃得更多，因为在吃饭时会有更高的愉悦感，或者更高的动机去获得寻找的食物。这些（享乐）过程被称为“喜欢”和“想要”。其次，人们会吃得更多，因为他们的生理系统无法快速关闭进食（导致大餐），或者因为食物无法在进食后抑制饥饿感。这最后两个过程被称为“饱足”和“饱足”。吃的乐趣可以分为两个部分：“喜欢”和“想要”。虽然这些术语经常一起出现，但它们是完全不同的。有时候，我们对自己非常喜欢的食物没有强烈的需求;有时候，我们对自己不太喜欢的食物有强烈的需求（例如土豆/斯台普斯）。重要的是，我们已经开发出了衡量喜欢和想要食物的程序。目前还不清楚过度消费是由于对某些食物的喜爱增加，还是由于对这些食物的需求增加。我们将确定在长时间的暴饮暴食中选择的食物类型，以及这是否在更大程度上是由增加的喜欢或想要驱动的。与此同时，重要的是能够测量控制膳食大小（饱足感）和导致进食后饥饿感减少（饱足感）的过程的实际变化。我们将确定饮食的哪个方面在允许暴饮暴食/大餐量或对饥饿的弱抑制中起主要作用。这将告诉我们如何使用特定的食物来控制这两个方面的饮食。能够将感觉和行为的变化与潜在的生理过程联系起来是很重要的。这意味着测量血液中已知与食欲控制有关的化学物质。这些化学物质中的一些被认为主要涉及饥饿（ghrelin）或饱腹感（GLP 1，CCK）或饥饿/饱腹感，喜欢和想要（瘦素）。因此，我们将评估这些信号影响过度消费的具体方式。从长远来看，过度消费会导致体重增加，而体重可能永远不会再减少，并可能损害健康。因此，我们开发了一个“安全”的过度消费模型，该模型来自刚刚完成的BBSRC项目。当超重和肥胖的人自愿参加一个为期12周的有监督的日常锻炼（固定能量消耗）计划时，一些人体重减轻，另一些人则没有。然而，独立于体重减轻，所有志愿者都显示心率下降，血压下降，健身增加（成为健康的关键）。这种反应差异背后的原因是，不减肥的不良反应者增加了食物摄入量，以抵消能量损失。这种增加可以解释为过度消费，相当于约290千卡/天。在缺乏锻炼的情况下，这将导致体重在一年内急剧增加超过6公斤。因此，我们可以使用这种“安全”的过度消费形式来检查潜在的行为驱动因素/喜欢和想要，饱足感和饱腹感/以及它们与信号肽的关联。这为调查食物行为的驱动因素提供了一种相关的长期方法。

This project will investigate the drivers of eating behaviour that occur during a prolonged period of overconsumption (excess intake of calories). Overconsumption is important as a major cause of weight (re)gain and obesity. The type of society which exists in many developed countries is said to represent an 'obesigenic' environment. This type of environment facilitates a high consumption of food (as well as encouraging sedentariness) and generates rapid weight gain that leads to obesity. The obesigenic environment 'offers' the possibility for people to overeat. People are able to eat too much of some foods because of excessive activation of hedonic (pleasure related) processes, or because of a defect in homeostatic processes. Firstly this means that people will eat more because of elevated sensations of pleasure during eating or heightened motivation to obtain a looked-for food. These (hedonic) processes are termed 'liking' & 'wanting'. Secondly, people will eat more because their physiological systems fail to shut off eating quickly (leading to large meals) or because food fails to suppress their hunger after eating. These last two processes are called 'satiation' and 'satiety'. The pleasure of eating can be divided into two components /'liking' & 'wanting'. Although these terms often occur together, they are quite different. Sometimes we do not have a strong wanting for foods that we like a lot; at other times we have a strong wanting for foods that are not especially liked (e.g. potatoes/food staples). Importantly, we have developed procedures that measure both the liking & wanting of foods. It is not known if overconsumption results from an increase in liking for certain foods, or from an increase in wanting for those foods. We will identify the types of foods selected during a prolonged period of overeating and whether this is driven to a greater degree by increased liking or wanting. At the same time it is important to be able to measure the actual changes in processes that control meal size (satiation) and which lead to the reduction of hunger after eating (satiety). We will identify which aspect of eating plays the major role in allowing overeating /a large meal size, or weak suppression of hunger. This will inform us how to use specific foods to control these two aspects of eating. It is important to be able to relate changes in sensations and behavior to underlying physiological processes. This means measuring chemicals in the blood that are known to be involved in appetite control. Some of these chemicals are thought to be involved mainly in hunger (ghrelin) or in satiety (GLP1, CCK) or in both hunger/satiety, liking & wanting (leptin). We will therefore assess the particular ways in which these signals influence overconsumption. Generating overconsumption in the long term leads to a gain in weight which may never be lost again and could impair health. We have therefore developed a 'safe' model of overconsumption that has arisen from a BBSRC project just finished. When overweight and obese people volunteer for a 12 week programme of supervised daily exercise (of fixed energy expenditure) some individuals lose weight and others do not. However, independent of weight loss all volunteers show decreases in heart rate, blood pressure, and an increase in fitness (key to becoming healthy). The reason behind this variability in response is that the poor responders who do not lose weight have increased their food intake to negate the energy lost. This increase can be interpreted as overconsumption and amounts to ~290 kcal/day. In absence of exercise this would lead to a dramatic weight increase of more than 6kg over a year. Therefore we can use this 'safe' form of overconsumption to examine changes in underlying behavioral drivers /liking & wanting, satiation and satiety/ and their association with signalling peptides. This provides a relevant long term method for investigating the drivers of food behaviour.