The role of dynorphins in energy homeostasis

强啡肽在能量稳态中的作用

• 批准号: nhmrc : 376021
• 负责人: A/Pr Amanda Salis
• 金额: $ 37.96万
• 依托单位: Garvan Institute of Medical Research
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2006
• 资助国家: 澳大利亚
• 起止时间: 2006-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/role-dynorphins-energy-homeostasis/98839
• 关键词: role; dynorphins; energy; homeostasis

While it is clear that carrying excess body weight can jeopardize your health, and that losing excess weight is good for you, attaining and maintaining a healthy body weight remains an elusive goal for more than 60 % of Australian adults. There are many barriers that make permanent weight loss difficult. One of the main biological barriers to weight loss is that humans aren t designed to diet. Instead, we vehemently conserve body fat whenever food is scarce. This leads to a Famine Reaction that contributes to nagging hunger, lethargy, loss of libido, reduced metabolic rate, plateaus, and rebound weight gain in response to weight loss programs of any kind. In a new 3-year project funded by the National Health and Medical Research Council of Australia, molecular scientists Dr Amanda Sainsbury-Salis and Associate Professor Herbert Herzog from the Garvan Institute endeavor to get to the root of the problem. Using cutting-edge molecular, genetic, and metabolic technology, Sainsbury-Salis and Herzog aim to identify the main culprits for the Famine Reaction. They hypothesize that the natural brain molecules neuropeptide Y and the endogenous morphine-like peptide dynorphin act together as major instigators of the Famine Reaction. Therefore they will determine whether mice that are deficient in these molecules can lose more weight in response to dietary restriction than normal mice. Moreover, they will determine whether dual deficiency of neuropeptide Y and dynorphin can not only reduce the voracious appetite that occurs during caloric restriction (eg: dieting), but whether it can also speed up metabolism and promote the loss of body fat. If their hypothesis proves correct, then it s likely that novel pharmaceutical agents that block the effects of neuropeptide Y and dynorphin could dramatically increase the do-ability and long-term effectiveness of lifestyle changes for permanent weight loss.

虽然很明显，携带多余的体重会危及你的健康，而减轻多余的体重对你有好处，但达到和保持健康的体重仍然是超过60%的澳大利亚成年人难以实现的目标。有许多障碍使永久减肥变得困难。减肥的主要生物学障碍之一是人类不是为了节食而设计的。相反，当食物稀缺时，我们会强烈地保存身体脂肪。这会导致饥饿反应，导致饥饿，嗜睡，性欲丧失，代谢率降低，高原，以及任何类型的减肥计划的反弹体重增加。在一个由澳大利亚国家健康和医学研究理事会资助的新的3年项目中，分子科学家阿曼达塞恩斯伯里-萨利斯博士和加文研究所的副教授赫伯特赫尔佐格奋进找到问题的根源。利用尖端的分子，遗传和代谢技术，Sainsbury-Salis和Herzog旨在确定饥荒反应的罪魁祸首。他们假设，自然的脑分子神经肽Y和内源性吗啡样肽强啡肽共同作用，作为饥饿反应的主要煽动者。因此，他们将确定缺乏这些分子的小鼠是否能比正常小鼠在饮食限制下减轻更多的体重。此外，他们将确定神经肽Y和强啡肽的双重缺乏是否不仅可以减少热量限制（例如：节食）期间发生的贪婪食欲，而且还可以加速新陈代谢，促进体脂的流失。如果他们的假设被证明是正确的，那么阻断神经肽Y和强啡肽作用的新型药物可能会大大增加改变生活方式以实现永久减肥的可行性和长期有效性。