ArticleJournal of neurochemistry2026
Dysregulation of Hippocampal Autophagic Machinery in the Activity-Based Anorexia Rat Model.
Article in Journal of neurochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
In Anorexia Nervosa (AN), the combination of self-induced starvation and hyperactivity may initially recruit the autophagic machinery to sustain the function of energy-demanding brain regions; however, its dysregulation may ultimately contribute to impaired brain function. We therefore investigated the autophagic machinery in the dorsal hippocampus (dHip), a central hub for energy status modulation and for cognitive processing, in the activity-based anorexia (ABA) rat model, the gold standard in the field. To analyze autophagic markers in the dHip, adolescent female Sprague-Dawley rats were exposed to 2 h/day of food access + free wheel access (ABA induction) and were sacrificed when they reached the maximum body weight loss allowed concomitantly with an increase in the running activity (acute phase) or following a 7-day recovery period. Our results show that ABA induction persistently disrupts the regulation of the autophagic machinery. In the acute phase, the ABA condition increases the phosphorylation of mTOR/ULK1 while promoting TFEB-associated mechanisms, enhancing the expression of autophagic markers such as Becn1, Ctsb genes, Beclin-1, and LC3-II proteins. After weight recovery, TFEB-induced activation of Becn1, Ctsb, Beclin-1, and LC3-II remains elevated. In addition, the enhanced expression of autophagic markers is accompanied by an increase in p62 and Caspase3, pro-apoptotic signals. Our findings reveal a sustained activation of autophagy across different stages of the ABA protocol. Rather than functioning exclusively as a survival mechanism, this process could evolve into a driver of aberrant behaviors typical of individuals with AN, such as dieting behaviors and hippocampal-dependent deficits.
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