Michael Harrop
Well-known member
https://jeatdisord.biomedcentral.com/articles/10.1186/s40337-025-01276-0
Abstract
Anorexia nervosa (AN) is a complex and serious mental disorder, which may affect individuals of all ages and sex, but primarily affecting young women. The disease is characterized by a disturbed body image, restrictive eating behavior, and a lack of acknowledgment of low body weight. The underlying causes of AN remain largely unknown, and current treatment options are limited to psychotherapy and nutritional support. This paper investigates the impact of Fecal Microbiota Transplants (FMT) from patients with AN on food intake, body weight, behavior, and gut microbiota into antibiotic-treated mice. Two rounds of FMT were performed using AN and control (CO) donors. During the second round of FMT, a subset of mice received gut microbiota (GM) from a different donor type. This split-group cross-over design was chosen to demonstrate any recovery effect of FMT from a non-eating disorder state donor. The first FMT, from donors with AN, resulted in lower food intake in mice without affecting body weight. Analysis of GM showed significant differences between AN and CO mice after FMT1, before cross-over. Specific bacterial genera and families Ruminococcaceae, Lachnospiraceae, and Faecalibacterium showed different abundances in AN and CO receiving mice. Behavioral tests showed decreased locomotor activity in AN mice after FMT1. After FMT2, serum analysis revealed higher levels of appetite-influencing hormones (PYY and leptin) in mice receiving AN-GM. Overall, the results suggest that AN-GM may contribute to altered food intake and appetite regulation, which can be ameliorated with FMT from a non-eating disorder state donor potentially offering FMT as a supportive treatment for AN.
Plain English summary
In our study, we explored whether characteristics associated with Anorexia Nervosa (AN), such as low body weight and altered appetite, could be transferred to mice pretreated with antibiotics through fecal transplants from individuals with AN. We used mice with antibiotic-depleted gut bacteria and humanized them by transplanting human donor gut microbiota. After observing reduced food intake in mice receiving AN gut microbiota, we conducted a second transplant with non-eating disorder donor microbiota to counteract these effects. We found that the food intake patterns of mice could be influenced by the type of microbiota they received after the first rounds of transplants, suggesting a potential for microbiota transplants to modify AN-related behaviors. Biomarker analysis indicated changes in appetite-regulating hormones in mice receiving AN microbiota, further supporting the role of gut microbiota in influencing eating behaviors. Our findings highlight the potential of microbiota transplants as a therapeutic approach for treating AN.
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