Biology subjects

Demangeat, T.

Publications and source records attributed to Demangeat, T..

3 recordsLinked to original sources

bioRxiv2026

Chronic Activity-Based Anorexia triggers a glial response in the hippocampus independent of intestinal epithelial Toll-Like Receptor 4

Anorexia nervosa is characterized by maladaptive eating behavior and cognitive dysfunction, which could be explained by a neuroinflammation. A gut dysbiosis could link gastrointestinal alterations to central dysfunctions, particularly via the toll-like receptor 4 (TLR4), which has been shown to play a key role in the activity-based anorexia (ABA) model. We aimed to evaluate the neuroinflammation and its behavioral consequences in the ABA model, and to decipher the role of the microbiota-gut-brain axis, and more specifically of TLR4, in these alterations of the central nervous system. We show that chronic restriction is more strongly associated with gut inflammation, cecal microbiota alteration and neuroinflammatory processes in the hippocampus than acute restriction. The hippocampal glial response is characterized by a loss of astrocyte density, and an increased number of deramified microglia. We further demonstrate that these alterations are independent of TLR4 expressed by intestinal epithelial cells. In conclusion, our results highlight that the chronicity of ABA-associated undernutrition alters the response of glial cells in the hippocampus that is linked with changes in microbiota composition, highlighting the importance of faster diagnosis and treatment of AN.

neuroscience↗

bioRxiv2025

Characterisation of changes in the gut microbiota associated with eating disorders

BackgroundEating disorders are serious pathologies that often begin in adolescence or young adulthood and persist for a significant period of time, with a strong negative impact on patients quality of life and mortality. The etiological origins of eating disorders are complex and involve both biological, psychological and societal factors. The gut microbiota was recently proposed as one of the potential factors involved in eating disorders. To gain a better understanding of the potential role of the gut microbiota in these diseases, we used 16S rRNA sequencing to compare the composition of the faecal microbiota of patients with all typical forms of eating disorders, i.e. anorexia nervosa, bulimia nervosa or binge-eating disorder, with that of healthy individuals. ResultsOur results demonstrate that each type of eating disorder is associated with a specific gut bacterial signature. We observed, for example, a decrease in the relative abundances of Agathobacter and Romboutsia genera and an increase in Pseudomonas in patients with anorexia, while patients with binge-eating disorder exhibit a decrease in the relative abundances of Akkermansia and Intestinimonas and an increase in Streptococcus, Eggerthella and Proteus. We also highlight a heterogeneity of gut microbiota composition in different subcategories of eating disorders, such as restricting versus binge-purge type anorexia or typical versus atypical binge-eating disorder. By focusing on the comorbidities reported by patients, we finally identified several bacterial taxa, such as Acidaminococcus and Eggerthella, whose level correlates with the occurrence of anxiety or depressive-like symptoms. ConclusionsTogether, our work demonstrates that eating disorders are associated with specific changes in gut microbiota composition and highlight the necessity to finely stratify patients to identify robust microbial signatures. In addition, we identified bacterial taxa correlating with comorbidities and decreased quality of life reported by patients. Our results now pave the way for determining the predictive value of the abundance of these taxa on the duration of the pathology or on the likelihood of relapse. They also constitute a valuable resource to further demonstrate the causal role of the gut microbiota in the onset or chronicisation of eating disorders.

microbiology↗

bioRxiv2024

Gut microbiota regulates food intake in a rodent model of binge-eating disorder

ObjectiveBinge-eating disorder is characterized by recurrent episodes of consumption of large amounts of food within a short period of time, without compensatory behaviours. This disease is a major public health issue since it decreases patients quality of life and is associated with numerous comorbidities, encompassing anxiety, depression and complications associated with obesity. The pathophysiology of binge-eating disorder is complex and involves both endogenous, environmental and sociocultural factors. The gut microbiota has been proposed to be an important player in the onset or maintenance of eating disorders. Here, we aim to better delineate the potential role of the gut microbiota in binge-eating disorder. MethodWe used a model of binge-eating disorder where eight-weeks-old C57Bl/6 female mice had access during 2 hours, every 2 days over a 10-day period, to a highly palatable and high-calorie diet. Half of the animals received antibiotics to deplete their gut microbiota. Eating behaviour and other behavioural parameters were compared between groups. ResultsWe observed an increase in food intake in mouse exposed to high-fat high-sucrose diet, as well as tachyphagia and craving for food during binge-eating episodes. We demonstrate the gut microbiota depletion further increases food intake, specifically during binge-eating episodes. DiscussionThese results show that the gut microbiota is involved in the control of food intake during episodes of binge-eating. This strengthens the potential role of the gut bacteria in binge-eating disorder and open the way for future therapeutic strategies aiming at targeting patients gut microbiota.

animal behavior and cognition↗