Brain’s ‘appetite control centre’ different in people who are overweight or living with obesity
剑桥大学的科学家们已经证明,超重和肥胖人群的下丘脑异于体重正常的人,而下丘脑是大脑中控制食欲的关键部位。
Cambridge scientists have shown that the hypothalamus, a key region of the brain involved in controlling appetite, is different in the brains of people who are overweight and people with obesity when compared to people who are a healthy weight.
剑桥研究人员称其发现进一步证明了大脑结构与体重和食物摄入的相关性。
The researchers say their findings add further evidence to the relevance of brain structure to weight and food consumption.
据估计,目前全球的超重或肥胖人数超过19亿。英国健康改善和差异办公室的数据显示,英国近三分之二的成年人超重或患有肥胖症。这增加了个人患上一系列健康问题的风险,包括2型糖尿病、心脏病和中风、癌症和精神健康问题。
Current estimations suggest that over 1.9 billion people worldwide are either overweight or obese. In the UK, according to the Office for Health Improvement & Disparities, almost two-thirds of adults are overweight or living with obesity. This increases an individual’s risk of developing a number of health problems, including type 2 diabetes, heart disease and stroke, cancer and poorer mental health.
我们的食量和食物类型受到多种因素影响,包括基因、激素调节和生活环境。目前人们还未彻底了解大脑传达饥饱信号的具体机制,不过研究表明,下丘脑——大脑中一个杏仁大小的区域——在其中发挥着重要作用。
A large number of factors influence how much we eat and the types of food we eat, including our genetics, hormone regulation, and the environment in which we live. What happens in our brains to tell us that we are hungry or full is not entirely clear, though studies have shown that the hypothalamus, a small region of the brain about the size of an almond, plays an important role.
剑桥大学精神病学系和露西·卡文迪许学院的斯蒂芬妮·布朗博士(Stephanie Brown)说:“虽然我们知道下丘脑对于食量大小有重要影响,但其实我们对这个人脑区域知之甚少。这是因为它非常小,很难通过传统的核磁共振脑部扫描来识别。”
Dr Stephanie Brown from the Department of Psychiatry and Lucy Cavendish College, University of Cambridge, said: “Although we know the hypothalamus is important for determining how much we eat, we actually have very little direct information about this brain region in living humans. That’s because it is very small and hard to make out on traditional MRI brain scans.”
大多数关于下丘脑食欲调节作用的证据来自动物研究。这些研究表明,下丘脑内部存在复杂的相互作用途径,不同的细胞群共同作用,告诉我们什么时候饿了,什么时候饱了。
The majority of evidence for the role of the hypothalamus in appetite regulation comes from animal studies. These show that there are complex interacting pathways within the hypothalamus, with different cell populations acting together to tell us when we are hungry or full.
为解决该问题,布朗博士和同事使用一种利用机器学习开发的算法,分析了1351名年轻人的核磁共振脑部扫描结果以及体重指数(BMI),通过对比体重过轻、健康体重、超重和肥胖的个体来寻找下丘脑的差异。
To get around this, Dr Brown and colleagues used an algorithm developed using machine learning to analyse MRI brain scans taken from 1,351 young adults across a range of BMI scores, looking for differences in the hypothalamus when comparing individuals who are underweight, healthy weight, overweight and living with obesity.
该小组刚刚在《Neuroimage: Clinical》杂志中发表的一篇研究指出,超重和肥胖的年轻人下丘脑的总体体积明显更大。确切地说,该小组发现下丘脑体积和体重指数(BMI)有重要关系。
In a study published recentlyin Neuroimage: Clinical, the team found that the overall volume of the hypothalamus was significantly larger in the overweight and obese groups of young adults. In fact, the team found a significant relationship between volume of the hypothalamus and body-mass index (BMI).
这种体积差异着重体现在下丘脑的部分子区域,它们通过释放激素来平衡饥饿感和饱腹感从而控制食欲。
These volume differences were most apparent in those sub-regions of the hypothalamus that control appetite through the release of hormones to balance hunger and fullness.
虽然该发现的意义尚不明确,比如结构变化是体重变化的原因还是结果,但研究人员认为这种变化可能与炎症有关。先前的动物研究表明,高脂肪饮食会引发下丘脑炎症,进而导致胰岛素抵抗和肥胖。仅仅三天的高脂肪饮食就足以引发老鼠的下丘脑炎症。而其他研究表明,这种炎症可以提高动物饱腹的阈值——也就是说,它们必须比平时吃更多的食物才有饱腹感。
While the precise significance of the finding is unclear – including whether the structural changes are a cause or a consequence of the changes in body weight – one possibility is that the change relates to inflammation. Previous animal studies have shown that a high fat diet can cause inflammation of the hypothalamus, which in turn prompts insulin resistance and obesity. In mice, just three days of a fat-rich diet is enough to cause this inflammation. Other studies have shown that this inflammation can raise the threshold at which animals are full – in other words, they have to eat more food than usual to feel full.
该研究的第一作者布朗博士补充道:“如果老鼠的实验结果也适用于人类,那么高脂肪饮食可能引发我们食欲控制中枢的炎症。随着时间的推移,这将改变我们对于饱腹感的判断能力以及身体的血糖处理能力,从而导致体重增加。”
Dr Brown, the study’s first author, added: “If what we see in mice is the case in people, then eating a high-fat diet could trigger inflammation of our appetite control centre. Over time, this would change our ability to tell when we’ve eaten enough and to how our body processes blood sugar, leading us to put on weight.”
研究小组表示,炎症可以解释个体下丘脑体积增加的原因。有观点认为,身体对炎症的反应是通过增加大脑中被称为神经胶质的特殊免疫细胞的大小来实现的。
Inflammation may explain why the hypothalamus is larger in these individuals, the team say. One suggestion is that the body reacts to inflammation by increasing the size of the brain’s specialist immune cells, known as glia.
该研究的资深作者、来自剑桥大学精神病学系和克莱尔学院的保罗·弗莱彻教授(Paul Fletcher)表示:“过去20年,我们对食欲控制以及肥胖如何影响食欲有了重要的认识。剑桥大学的代谢研究人员在这方面发挥了主导作用。”
Professor Paul Fletcher, the study’s senior author, from the Department of Psychiatry and Clare College, Cambridge, said: “The last two decades have given us important insights about appetite control and how it may be altered in obesity. Metabolic researchers at Cambridge have played a leading role in this."
“我们希望采用这种新方法来分析大型数据库中的脑部扫描结果,可以将这项工作进一步扩展到人类身上,最终将这些微妙的大脑结构发现与食欲和饮食的变化联系起来,更全面地理解肥胖。”
“Our hope is that by taking this new approach to analysing brain scans in large datasets, we can further extend this work into humans, ultimately relating these subtle structural brain findings to changes in appetite and eating and generating a more comprehensive understanding of obesity.”
研究小组表示,需要进一步研究以确定是超重导致下丘脑体积的增加,还是下丘脑体积较大的人本身就食量更大。这两个因素也可能相互作用,形成一个反馈循环。
The team say more research is needed to confirm whether increased volume in the hypothalamus is a result of being overweight or whether people with larger hypothalami are predisposed to eat more in the first place. It is also possible that these two factors interact with each other causing a feedback loop.
这项研究得到了伯纳德‧沃尔夫卫生神经科学基金会(Bernard Wolfe Health Neuroscience Fund)、Wellcome和NIHR剑桥生物医学研究中心的支持,并得到了英国阿尔茨海默症研究中心的额外资助。
The research was supported by the Bernard Wolfe Health Neuroscience Fund, Wellcome and the NIHR Cambridge Biomedical Research Centre, with additional funding from Alzheimer’s Research UK.