Abstract
Restrictive anorexia nervosa is associated with reduced eating and severe body weight loss leading to a cachectic state. Hypothalamus plays a major role in the regulation of food intake and energy homeostasis. In the present study, alterations of hypothalamic proteome and particularly of proteins involved in energy and mitochondrial metabolism have been observed in female activity-based anorexia (ABA) mice that exhibited a reduced food intake and a severe weight loss. In the hypothalamus, mitochondrial dynamic was also modified during ABA with an increase of fission without modification of fusion. In addition, increased dynamin-1, and LC3II/LC3I ratio signed an activation of autophagy while protein synthesis was increased. In conclusion, proteomic analysis revealed an adaptive hypothalamic protein response in ABA female mice with both altered mitochondrial response and activated autophagy.
Highlights
Anorexia Cachexia Syndrome (ACS) is characterized by a reduced food intake and a body weight loss due to a reduction of fat and lean mass[1]
Mice were randomized into 3 groups: an activity-based anorexia group (ABA), a limited-food access group (LFA) and an ad libitum group (Control)
ABA mice were placed in cages with an activity wheel, while both LFA and Control mice were placed in standard cages
Summary
Anorexia Cachexia Syndrome (ACS) is characterized by a reduced food intake and a body weight loss due to a reduction of fat and lean mass[1]. In response to peripheral and hormonal signals, hypothalamic neuronal activity and transmitter release are modified such as orexigenic and anorexigenic neuropeptide release leading to the regulation of food intake and energy homeostasis[16]. Proteomic profiling of the hypothalamus have been performed in different animal models to study body weight homeostasis. In the present paper, we aimed to evaluate hypothalamic proteome and identified altered biological process in ABA model associating a spontaneous reduced food intake and a severe body weight loss
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