The role of leptin within the substantia nigra and lateral hypothalamus in suppression of hyperactivity in activity-based anorexia model.

Abstract

Anorexia nervosa (AN) is an eating disorder characterized by a pursuit for thinness and compulsive thoughts about nutrition, body shape, and weight. Hyperactivity has also been recognized as a key symptom associated with AN, impacting chronicity and complications. Leptin, a hormone produced by white adipocytes, plays a role in regulating appetite and energy homeostasis. Leptin has emerged as a potential therapeutic target for reducing hyperactivity in AN, as leptin has showed to reduce activity levels in animal models for AN. This study aimed to investigate the role of leptin within the substantia nigra (SN) and lateral hypothalamus (LH) in suppressing hyperactivity without impacting food intake using the activity based anorexia model (ABA-model). Limited research time permitted the assessment of only the lateral hypothalamus. The findings indicate that leptin infusions in the LH did not significantly reduce hyperactivity or food intake during the ABA-model, challenging the hypothesized outcomes. The absence of explicit exclusion criteria and histological validation for infusion sites may have influenced the results. Despite the non-significant findings, this study contributes to understanding leptin’s role in AN. Previous clinical case studies suggest potential beneficial effects of leptin on reducing inner restlessness, anxiety and depressed mood in AN. These findings underscore leptin’s broader impact beyond modulating physical symptoms, highlighting its potential as a therapeutic intervention for addressing both physical and psychological aspects of AN. Further clinical research is warranted to elucidate leptin’s effect in AN patients and to develop targeted treatment strategies.