Metabolic signatures and neurophysiological mechanisms of bad food decisions.

不良食物决策的代谢特征和神经生理学机制。

基本信息

项目摘要

Vertebrate and invertebrate species have to deal with changes in food availability in order to keep a positive energy balance. A well-balanced energy homeostasis is indispensable for the individual´s health. An increased intake of energy-dense food or an increase in physical inactivity are fundamental causes of obesity and overweight. On the other side hunger or malnutrition induces painful sensation caused by insufficient caloric intake leading to extensive physiological changes up to organ damage and death. At a certain point, progressive malnutrition evokes the individual´s inevitable decision to intake food of bad quality which is normally avoided. Our project aims to understand what kind of changes occur in brain-body communication to induce the intake of bad quality food, that is normally avoided. We aim to identify the metabolic signatures and neurophysiological mechanisms that triggers bad food decisions. Interestingly, we assume that the underlying changes also occur in obesity, the other extreme of malnutrition. Therefore, we aim a holistic understanding of bad feeding decisions on a metabolic, neurophysiological, and endocrinological level. The project will exploit the experimental potential of Drosophila to study the metabolic and neurophysiological basis of bad food decisions. We will combine a multiomics strategy (metabolomics, transcriptomics and proteomics) with neurogenetics (e.g. optogenetics), behavioral studies, high resolution microscopy and live cell imaging (Ca2+ and FRET imaging) and are convinced that this scientific approach will provide new insights into the mechanisms of bad food decisions. Targeting mechanisms underlying hunger-driven eating behavior including bad food decisions may help to advance therapeutic strategies by improving patients´ compliance to body weight loss interventions.
脊椎动物和无脊椎动物物种必须应对食物供应的变化,以保持正能量平衡。均衡的能量平衡对于S的健康是不可或缺的。高能量食物摄入量的增加或身体活动不足的增加是肥胖和超重的根本原因。另一方面,饥饿或营养不良会引起卡路里摄入不足引起的痛感,导致广泛的生理变化,直至器官受损和死亡。在某种程度上,进行性营养不良会唤起S不可避免的决定,吃质量不好的食物,而这通常是避免的。我们的项目旨在了解在大脑和身体的交流中发生了什么样的变化来诱导人们摄入通常可以避免的劣质食物。我们的目标是确定引发不良食物决定的代谢特征和神经生理机制。有趣的是,我们假设潜在的变化也发生在肥胖症上,这是营养不良的另一个极端。因此,我们的目标是从代谢、神经生理和内分泌水平全面了解不良喂养决定。该项目将利用果蝇的实验潜力,研究不良食物决定的代谢和神经生理学基础。我们将结合多元组学(代谢组学、转录组学和蛋白质组学)与神经遗传学(例如光遗传学)、行为研究、高分辨率显微镜和活细胞成像(钙离子和FRET成像)相结合,并相信这种科学方法将为不良食物决定的机制提供新的见解。饥饿驱动进食行为的靶向机制,包括不好的食物决定,可能有助于通过改善患者对减肥干预的依从性来推进治疗策略。

项目成果

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Professor Dr. Peter Kovacs其他文献

Professor Dr. Peter Kovacs的其他文献

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{{ truncateString('Professor Dr. Peter Kovacs', 18)}}的其他基金

Rolle von Vaspin in der Pathogenese von Typ 2 Diabetes und Adipositas
Vaspin 在 2 型糖尿病和肥胖发病机制中的作用
  • 批准号:
    109669813
  • 财政年份:
    2008
  • 资助金额:
    --
  • 项目类别:
    Research Grants

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