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Bu sayfa, 26. Dünya Psikiyatri Kongresi'nde sunulan çalışmanın yapay zekâ desteğiyle hazırlanmış Türkçe özetidir. Çalışmanın sahibi sunan yazarlardır; atıf için orijinal kaynağa başvurun.

SO332

Metabolic regulation of synaptic plasticity in anorexia nervosa

METABOLIC REGULATION OF SYNAPTIC PLASTICITY IN ANOREXIA NERVOSA

Anorexia nervosa is conceptualized as a metabo-psychiatric disorder arising from the interaction between metabolic traits and plastic neural circuits, suggesting that treatment should target both metabolic physiology and brain-based processes.

The aim of this study is to present a conceptual framework illustrating how metabolic biology and neural circuit function are intertwined in anorexia nervosa (AN). The authors reviewed hypothalamic, striatal, prefrontal, and limbic circuits that integrate metabolic, emotional, and cognitive information, reporting that all exhibit altered plasticity during starvation. Table 1 in the poster summarizes the synaptic effects of systemic metabolic signals: glucose influences neuronal excitability by regulating excitatory synaptic plasticity in feeding circuits; insulin shifts LTP/LTD (long-term potentiation/long-term depression) thresholds and AMPA/NMDA signaling in a PI3K-dependent manner; beta-hydroxybutyrate induces histone acetylation and increases hippocampal BDNF through HDAC inhibition; ghrelin increases dendritic spine density and LTP; and leptin, peptide YY, estradiol, adiponectin, cortisol, and the GH/IGF-1 axis remodel feeding circuits as part of the endocrine profile specific to starvation. At the molecular level, the AMPK, mTOR, and O-GlcNAc pathways are described as intracellular metabolic sensors that translate nutrient availability into changes in protein synthesis, receptor trafficking, and dendritic spine structure (Figure 2). Genetic evidence links AN to heritable metabolic traits, suggesting that metabolic predisposition contributes to disease risk. The poster contains no numerical results or statistical comparisons, instead presenting a conceptual synthesis. In conclusion, understanding how metabolic signals reshape synaptic ensembles sheds light on mechanisms of susceptibility and points to targets for interventions that could restore adaptive plasticity.

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