SSA: Run, eat, sleep, repeat: Hypothalamic integration of homeostatic and circadian signals

保持有规律的体育锻炼、饮食和睡眠被认为是享受健康长寿的关键。这样的时间表可以加强我们的24小时生物钟，确保它与我们的社会和物理环境保持最佳一致。反过来，生物钟调节大脑中控制我们吃多少和睡多少的部分。这些大脑区域还与生物钟进行通信，以便我们在白天和晚上的正确时间开始和结束我们的饮食和睡眠周期。日常行为模式的中断，例如轮班工作，对我们的健康有害，削弱了我们的生物钟，改变了我们锻炼，吃饭和睡觉的时间以及我们吃多少，喝多少，休息。这导致体重过度增加，心脏和精神健康状况不佳。大脑的下丘脑既包含生物钟，也包含调节我们吃多少和睡多少的中心。不幸的是，大脑中用来在生物钟和下丘脑的其他关键区域之间进行交流的化学物质是未知的。一个很好的候选者是大脑的黑皮质素系统，在这个项目中，学生将使用小鼠和研究如何激活或抑制黑皮质素信号在下丘脑影响其控制，如果，什么时候和多少我们吃，睡，和锻炼。此外，将探讨改变这种大脑化学物质对模拟轮班工作的反应的影响。预计这种化学信号的一些变化将有助于重新调整轮班工作时间表的变化。这项小鼠工作将通过使用英国生物库进行补充，并评估人类大脑中黑皮质素信号的改变是否对睡眠，身体活动和幸福感有类似的影响。这可能会导致与药物的发展有用的打击长期的健康后果轮班工作。

Maintaining regular patterns of physical exercise, meals, and sleep are accepted as key to enjoying a long and healthy life. Such schedules act to strengthen our 24h body clock, ensuring that it is optimally aligned with our social and physical environment. In turn, the body clock regulates parts of the brain that control how much we eat and sleep. These brain areas also communicate with the body clock so that we initiate and terminate our meals and sleep cycles at the right times of the day and night. Disruptions to daily patterns in behavior, such as occurs with shiftwork, are detrimental to our health, weakening our body clock and altering both the time of day at which we exercise, eat, and sleep as well how much we eat, drink, and rest. This results in excessive body weight gain and poor heart and mental health.The brain's hypothalamus contains both the body clock as well as the centres that regulate how much we eat and sleep. Unfortunately, the brain chemical that it is used to communicate between the body clock and these other key areas of the hypothalamus is unknown. A good candidate is the brain's melanocortin system and in this project, the student will use mice and study how activating or inhibiting melanocortin signaling within the hypothalamus affects its control of if, when and how much we eat, sleep, and exercise. Further, the effects of altering this brain chemical on the response to simulated shiftwork will be explored. It is anticipated that some changes with this chemical signal will facilitate re-adjustment to changes in shift-work schedules. This mouse work will be complemented by using the UK biobank and evaluating if alterations in melanocortins signaling in the human brain have similar effects on sleep, physical activity, and well-being. This could result with the development of agents useful to combat the long-term health consequences of shiftwork.