Normandie University, UNIROUEN, Nutrition, Gut and Brain Laboratory Rouen, France; Normandie University, UNIROUEN, Institute for Research and Innovation in Biomedicine (IRIB), Rouen, France; Nutrition Department, Rouen University Hospital, Rouen, France.
Normandie University, UNIROUEN, Nutrition, Gut and Brain Laboratory Rouen, France; Normandie University, UNIROUEN, Institute for Research and Innovation in Biomedicine (IRIB), Rouen, France.
Nutrition. 2019 Nov-Dec;67-68:110557. doi: 10.1016/j.nut.2019.110557. Epub 2019 Aug 5.
Activity-based anorexia (ABA) in rodents is a behavioral model of anorexia nervosa, characterized by negative energy balance, hyperactivity, and dysbiosis of gut microbiota. Gut bacteria are known to produce energy substrates including adenosine triphosphate (ATP) and acetate. The aim of this study was to determine whether ABA alters the proteome of gut microbiota relevant to ATP and acetate production.
The ABA was developed in male mice and compared with food-restricted and ad libitum-fed conditions. Proteomic analysis of feces was performed using the two-dimentional gel electrophoresis and mass spectrometry. The in vitro ATP-producing capacity of proteins extracted from feces was assayed.
Increased levels of the phosphoglycerate kinase, an ATP-producing glycolytic enzyme, was detected in feces of food-restricted mice and this enzyme was further increased in the ABA group. Starvation also upregulated several other proteins synthetized by order Clostridiales including Clostridiaceae and Lachnospiraceae families. No significant differences in the in vitro ATP-producing capacity by bacterial proteins from ABA, food-restricted, and ad libitum-fed control mice were found. However, plasma levels of acetate strongly tended to be increased in the activity groups including ABA mice.
The data revealed that starvation in food-restricted and ABA mice induced proteome modification in gut bacteria favoring ATP production mainly by the order Clostridiales. However, this did not result in increased total ATP-production capacity by gut microbiota. These changes can be interpreted as an adaptation of specific gut bacteria to the host malnutrition beneficial for host survival.
活动相关厌食症（ABA）在啮齿动物中是厌食症的行为模型，其特征为负能量平衡、过度活跃和肠道微生物群落失调。已知肠道细菌会产生包括三磷酸腺苷（ATP）和乙酸盐在内的能量底物。本研究旨在确定 ABA 是否会改变与 ATP 和乙酸盐产生相关的肠道微生物群的蛋白质组。
ABA 在雄性小鼠中建立，并与限制食物和随意进食条件进行比较。使用二维凝胶电泳和质谱法对粪便进行蛋白质组分析。从粪便中提取的蛋白质的体外 ATP 产生能力进行了测定。
在限制食物的小鼠粪便中检测到磷酸甘油酸激酶（一种产生 ATP 的糖酵解酶）水平升高，该酶在 ABA 组中进一步增加。饥饿还上调了其他几种由梭状芽胞杆菌属（Clostridiales），包括梭菌科和毛螺菌科产生的蛋白质。从 ABA、限制食物和随意进食的对照小鼠的粪便中提取的细菌蛋白质的体外 ATP 产生能力没有明显差异。然而，ABA 等活动组的血浆乙酸盐水平有强烈的上升趋势。
数据显示，限制食物和 ABA 小鼠的饥饿诱导了肠道细菌的蛋白质组修饰，有利于 ATP 的产生，主要通过梭状芽胞杆菌属（Clostridiales）。然而，这并没有导致肠道微生物群总 ATP 产生能力的增加。这些变化可以解释为特定肠道细菌对宿主营养不良的适应，有利于宿主的生存。
