SFB 1052: Obesity Mechanisms

SFB 1052：肥胖机制

• 批准号: 209933838
• 金额: --
• 依托单位: Universität Leipzig
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2013
• 资助国家: 德国
• 起止时间: 2012-12-31 至 2023-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/209933838?language=en
• 关键词: SFB; 1052; Obesity; Mechanisms

The prevalence of obesity (in Germany: 24%) has increased worldwide by pandemic dimensions in recent decades, and it represents a major health challenge to many societies. Besides musculoskeletal or lung disorders caused by being overweight, obesity as a metabolic disorder also increases the risk of cardiovascular disease, type 2 diabetes, Alzheimer’s disease, depression, and some types of cancer, thereby contributing to a decline in quality of life and life expectancy. Obesity is a multifactorial disorder influenced by a combination of genetic, behavioral, life style and environmental factors, including control of appetite, satiety and energy expenditure, availability and nutritional content of food. Because the factors (and their interaction) causing obesity are only incompletely understood, weight loss strategies may not address the underlying causes of energy imbalance. Therefore, the ultimate long-term aim of the Collaborative Research Centre (CRC) 1052: “Obesity Mechanisms” is to define novel targets and mechanisms for future therapeutic approaches in the treatment of obesity. There are several questions about the unresolved, pathogenic mechanisms of obesity and its comorbid disorders, three of which are central and unifying to this Collaborative Research Centre:1. What are the central mechanisms for overeating in the development of obesity?2. How does overeating lead to adverse fat deposition and adipose tissue inflammation?3. Which fat-derived “signals” (adipokines) contribute to obesity-related diseases?In three main research areas, we aim to unravel complex mechanisms in the control of energy homeostasis by the central nervous system (A, Overeating), the determination of adverse fat deposition and its associated adipose tissue dysfunction and inflammation (B, Fat Deposition and Inflammation), and the regulation and effects of altered adipokine secretion in obesity (C, Adipokines).

近几十年来，肥胖症的患病率（在德国：24%）在世界范围内以流行病的形式增加，并且它代表了许多社会的主要健康挑战。除了由超重引起的肌肉骨骼或肺部疾病外，肥胖作为一种代谢紊乱还增加了心血管疾病、2型糖尿病、阿尔茨海默病、抑郁症和某些类型的癌症的风险，从而导致生活质量和预期寿命下降。肥胖是一种多因素疾病，受遗传、行为、生活方式和环境因素的影响，包括食欲控制、饱腹感和能量消耗、食物的可获得性和营养成分。由于导致肥胖的因素（及其相互作用）还不完全清楚，减肥策略可能无法解决能量失衡的根本原因。因此，协作研究中心（CRC）1052：“肥胖机制”的最终长期目标是为未来治疗肥胖症的治疗方法定义新的靶点和机制。关于肥胖及其共病疾病的未解决的致病机制有几个问题，其中三个是这个合作研究中心的核心和统一：1。 暴饮暴食导致肥胖的主要机制是什么？2. 暴饮暴食如何导致不良脂肪沉积和脂肪组织炎症？3. 哪些脂肪衍生的“信号”（脂肪因子）导致肥胖相关疾病？在三个主要的研究领域，我们的目标是解开复杂的机制，在控制能量稳态的中枢神经系统（A，暴饮暴食），确定不利的脂肪沉积及其相关的脂肪组织功能障碍和炎症（B，脂肪沉积和炎症），和调节和影响改变脂肪因子分泌肥胖（C，脂肪因子）。