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Disrupted intestinal microbiota contributes to the pathogenesis of anorexia nervosa (Part 2)

ABSTRACT: Anorexia nervosa (AN) is an eating disorder with a high mortality affecting about 0.5% of women, where no evidence-based effective treatment exists. The pathogenesis likely involves genetic and environmental alterations. We hypothesized that a disrupted gut microbiota contributes to AN pathology. In analyses comparing 70 AN with 77 healthy females, we found multiple taxa, functional modules, structural variants and growth rates of bacterial gut microbiota, and viral gut microbiota that were altered in AN with parts of these perturbations linked to estimates of eating behavior and mental health. In silico, causal inference analyses implied bacterial metabolites mediated parts of the impact of altered gut microbiota on AN behavior, and in vivo, fecal microbiota transplantation from AN cases to germ-free mice induced a lower body weight and hypothalamic and adipose tissue gene expressions related to aberrant energy metabolism and eating and mental behavior.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Blood

DISEASE(S): Anorexia Nervosa

SUBMITTER: Aidan McGlinchey

PROVIDER: ST002495 | MetabolomicsWorkbench | Wed May 18 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

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Disrupted intestinal microbiota contributes to the pathogenesis of anorexia nervosa (Part 1)

Project description:Anorexia nervosa (AN) is an eating disorder with a high mortality affecting about 1% of women, where no evidence-based effective treatment exists. The pathogenesis likely involves genetic and environmental alterations. We hypothesized that a disrupted gut microbiota contributes to AN pathogenesis. In analyses comparing 70 AN with 77 healthy females, we found multiple taxa, functional modules, structural variants and growth rates of bacterial gut microbiota, and viral gut microbiota that were altered in AN with parts of these perturbations linked to estimates of eating behavior and mental health. In silico, causal inference analyses implied serum bacterial metabolites mediated parts of the impact of altered gut microbiota on AN behavior, and in vivo, three independent fecal microbiota transplantation from AN cases to germ-free mice under energy restricted feeding mirroring AN eating behavior consistently induced a lower body weight gain and hypothalamic and adipose tissue gene expressions related to aberrant energy metabolism and eating and mental behavior.

2022-05-18 | ST002494 | MetabolomicsWorkbench

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Project description:The gut microbiome is significantly altered in inflammatory bowel diseases, but the basis of these changes is not well understood. We have combined metagenomic and metatranscriptomic profiling of the gut microbiome to assess changes to both bacterial community structure and transcriptional activity in a mouse model of colitis. Gene families involved in microbial resistance to oxidative stress, including Dps/ferritin, Fe-dependent peroxidase and glutathione S-transferase, were transcriptionally up-regulated in colitis, implicating a role for increased oxygen tension in gut microbiota modulation. Transcriptional profiling of the host gut tissue and host RNA in the gut lumen revealed a marked increase in the transcription of genes with an activated macrophage and granulocyte signature, suggesting the involvement of these cell types in influencing microbial gene expression. Down-regulation of host glycosylation genes further supports a role for inflammation-driven changes to the gut niche that may impact the microbiome. We propose that members of the bacterial community react to inflammation-associated increased oxygen tension by inducing genes involved in oxidative stress resistance. Furthermore, correlated transcriptional responses between host glycosylation and bacterial glycan utilisation support a role for altered usage of host-derived carbohydrates in colitis. Complementary transcription profiling data from the mouse hosts have also been deposited at ArrayExpress under accession number E-MTAB-3590 ( http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3590/ ).

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