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SEX-SPECIFIC MODULATION OF THE GUT–BRAIN AXIS BY PROBIOTICS IN A MOUSE MODEL OF BINGE EATING DISORDER
Luciene Vieiraand 7 co-authors
Universidade Federal de Minas Gerais
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-018
Presentation
Date TBA
Board: PS02-07PM-018
Event Information
Poster Board
PS02-07PM-018
Poster
View posterAbstract
Binge eating disorder (BED) is characterized by recurrent binge eating episodes occurring at least once per week for a minimum of three months and is frequently associated with psychiatric comorbidities such as anxiety and depression. Lisdexamfetamine is currently the only approved pharmacological treatment for BED; however, its use is limited by side effects and abuse potential. In this context, the gut–brain–microbiota axis has emerged as a promising therapeutic target, given the role of intestinal microorganisms in metabolic regulation and mental health, including appetite control and eating behavior. We evaluated the effects of the probiotic Lacticaseibacillus rhamnosus 64 (L64) on metabolic, biochemical, behavioral, and neuroinflammatory parameters in a C57BL/6 mouse model of BED. Male and female mice (6–7 weeks old) were subjected to a BED protocol consisting of 12 feeding sessions of 2 hours each, during which food intake was measured. Animals received treatment with L64, saline, or fluoxetine. Outcome measures included body weight, adiposity index, fasting glucose levels, anxiety-, compulsivity-, and depression-like behaviors, striatal glutamatergic neurotransmission, and inflammatory parameters. Both male and female mice developed binge eating behavior; however, increased anxiety- and compulsivity-like behaviors were observed exclusively in females. Treatment with L64 reduced food intake, improved metabolic parameters, and attenuated compulsive-like behavior in female mice. These findings indicate increased behavioral vulnerability to BED in females and suggest that modulation of the gut–brain axis via L64 may represent a promising therapeutic strategy to mitigate the metabolic and behavioral consequences associated with BED.
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