ESPEN 2020 Abstract Submission

Topic: Nutrition and chronic disease

Abstract Submission Identifier: ESPEN20-ABS-1565

GUT MICROBIOTA ALTERATION IN A MOUSE MODEL OF ANOREXIA NERVOSA

J. Breton ^{1, 2}, P. Tirelle ², S. Hasanat ², A. Pernot ², C. L'Huillier ², J.-C. Do Rego ³, P. Déchelotte ^{1, 2}, M. Coëffier ^{1, 2}, L. B. Bindels ⁴, D. Ribet^*, ²

¹Nutrition Department, Rouen University Hospital, ²INSERM UMR1073, ³Animal Behavior Platform, SCAC, UNIROUEN, Université de Rouen, ROUEN, France, ⁴Metabolism and Nutrition Research Group, Université catholique de Louvain, BRUSSELS, Belgium

Rationale: Anorexia Nervosa is a severe disease depending on both biological, psychological and environmental factors. The gut microbiota has recently been proposed as one of the biological factors potentially involved in the onset or maintenance of Anorexia Nervosa (1). To unravel the potential role of the gut microbiota in this disease, we characterized the dysbiosis occurring in a mouse model of Anorexia combining food restriction and physical activity. We then correlated bacteria level changes with different physiological parameters such as body weight, food intake or levels of hypothalamic neuropeptides.

Methods: 8-weeks old C57Bl/6JRj male mice (n=6-8/group) were either fed ad libitum (control group) or had a restricted access to food (3h per day) combined with a free access to a running wheel (Activity-based Anorexia (ABA) group). We collected mice cecal contents at the end of the protocol and characterized the gut microbiota alteration in ABA mice by combining 16S rRNA gene sequencing and quantitative PCR analyses of targeted genera or species.

Results: We identified 68 amplicon-sequence variants (ASVs) with decreased levels and 8 ASVs with increased levels in the cecal content of ABA mice compared to control mice. We observed in particular in ABA mice increases in the abundance of Clostridium cocleatum (x11.9 versus control mice, P<0.05) and several Lactobacillus species (x3.1-7.4 versus control mice, P<0.05) and a decrease in the abundance of Burkholderiales (x0.4 versus control mice, P<0.05). Interestingly, we show that most of the observed gut microbiota alterations (>90%) are due to food restriction and are not affected by physical activity. In addition, we identified several bacterial groups that correlate with mice body weight, food intake, lean and fat masses as well as with hypothalamic mRNA levels of NPY (Neuropeptide Y) and POMC (Pro-opiomelanocortin).

Conclusion: Our study provides a comprehensive characterization of the gut microbiota dysbiosis occurring in the Activity-Based Anorexia mouse model. These data constitute a valuable resource to further decipher the role of the gut microbiota in the different facets of anorexia pathophysiology, such as functional gastrointestinal disorders, appetite regulation and mood disorders.

References: (1) Breton J, Déchelotte P, Ribet D. Intestinal microbiota and anorexia nervosa. Clinical Nutrition Experimental. 2019;28:11-21.

Disclosure of Interest: J. Breton: None Declared, P. Tirelle: None Declared, S. Hasanat: None Declared, A. Pernot: None Declared, C. L'Huillier: None Declared, J.-C. Do Rego: None Declared, P. Déchelotte Other: Co-founder of the TargEDys company, M. Coëffier: None Declared, L. Bindels: None Declared, D. Ribet: None Declared

Keywords: Eating disorders, Gut microbiota