Food for Health Ireland, University College Cork, Cork, Ireland.
Psychoneuroendocrinology. 2012 Jun;37(6):729-41. doi: 10.1016/j.psyneuen.2011.06.015. Epub 2011 Jul 23.
Chronic stress and diet can independently or in concert influence the body's homeostasis over time. Thus, it is crucial to investigate the interplay of these parameters to gain insight into the evolution of stress-induced metabolic and eating disorders.
C57BL/6J mice were subjected to chronic psychosocial (mixed model of social defeat and overcrowding) stress in combination with either a high- or low-fat diet for three or six weeks. To determine the evolution of stress and dietary effects, changes in body weight, caloric intake and caloric efficiency were determined as well as circulating leptin, insulin, glucose and corticosterone levels and social avoidance behaviour.
Exposure to stress for three weeks caused an increase in weight gain, in caloric intake and in caloric efficiency only in mice on a low-fat diet. However, after six weeks, only stressed mice on a high-fat diet displayed a pronounced inhibition of body weight gain, accompanied by reduced caloric intake and caloric efficiency. Stress decreased circulating leptin levels in mice on a low-fat diet after three weeks and in mice on a high-fat diet after three and six weeks of exposure. Plasma levels of insulin and markers of insulin resistance were blunted in mice on high-fat diet following six weeks of stress exposure. Social avoidance following chronic stress was present in all mice after three and six weeks.
This study describes the evolution of the chronic effects of social defeat/overcrowding stress in combination with exposure to high- or low-fat diet. Most importantly, we demonstrate that a six week chronic exposure to social defeat stress prevents the metabolic effects of high-fat diet, by inhibiting an increase in weight gain, caloric intake and efficiency and insulin resistance as well as in plasma leptin and insulin levels. This study highlights the importance of considering the chronic aspects of both parameters and their time-dependent interplay.
慢性应激和饮食可以独立或协同作用,随着时间的推移影响身体的内稳态。因此,研究这些参数的相互作用对于深入了解应激引起的代谢和饮食失调的演变至关重要。
C57BL/6J 小鼠接受慢性心理社会(社会挫败和过度拥挤的混合模型)应激,同时接受高脂肪或低脂肪饮食,持续 3 或 6 周。为了确定应激和饮食影响的演变,测定了体重、热量摄入和热量效率的变化,以及循环瘦素、胰岛素、葡萄糖和皮质酮水平和社会回避行为。
暴露于应激 3 周会导致体重增加、热量摄入增加和热量效率增加,但仅在低脂饮食的小鼠中增加。然而,6 周后,只有高脂肪饮食的应激小鼠表现出明显的体重增加抑制,伴随着热量摄入和热量效率降低。应激 3 周后,低脂饮食的小鼠循环瘦素水平降低,3 和 6 周后,高脂肪饮食的小鼠循环瘦素水平降低。高脂肪饮食的应激 6 周后,血浆胰岛素和胰岛素抵抗标志物水平降低。慢性应激后的社会回避在所有小鼠中持续存在 3 和 6 周。
本研究描述了社会挫败/过度拥挤应激与暴露于高脂肪或低脂肪饮食相结合的慢性影响的演变。最重要的是,我们证明了 6 周的慢性社会挫败应激暴露可以防止高脂肪饮食的代谢影响,通过抑制体重增加、热量摄入和效率以及胰岛素抵抗以及血浆瘦素和胰岛素水平的增加来实现。本研究强调了考虑这两个参数的慢性方面及其随时间变化的相互作用的重要性。