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  1. Philip J Smith
  1. Department of Gastroenterology, Royal Liverpool Hospital, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK
  1. Correspondence to Dr Philip J Smith, Department of Gastroenterology, Royal Liverpool Hospital, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK; philip.smith{at}liverpoolft.nhs.uk

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Basic science

New insights into the contribution of the gut microbiome to irritable bowel syndrome

Mars R, Yang Y, Ward T, et al. Longitudinal multi-omics reveals subset-specific mechanisms underlying irritable bowel syndrome. Cell 2020;182:1460–73.e17. doi: 10.1016/j.cell.2020.08.007.

While perturbation of the composition of the gut microbiome has been previously observed in patients with irritable bowel syndrome (IBS), the specific mechanisms by which this may contribute to the onset or progression of the condition are not well defined. To explore this further, researchers performed longitudinal analysis (over 6 months) of samples collected from 77 well-phenotyped IBS patients and healthy controls; this was primarily via stool and serum analysis, but also via colonic biopsy in approximately half of participants. Samples were analysed by systems biology techniques which evaluated both host mucosa and gut microbiome function (including shotgun metagenomics, metabonomics, transcriptomics and epigenetics), and an integrative multiomics approach was used to interrogate data. Distinctive patterns of alterations in metabolites derived from gut microbial activity were found to characterise different IBS subtypes, with reduced short-chain fatty acids observed in those with IBS and constipation, while an increase in both tryptamine and primary bile acids was identified in those with diarrhoea-variant IBS. However, of greatest interest was the novel finding of a reduction in faecal hypoxanthine in patients with both main variants of IBS compared with controls, and the subsequent demonstration of increased degradation of purine nucleotides by both the gut microbiome and the host mucosa in IBS. The researchers concluded that such ‘purine starvation’ in IBS may result in a reduced source of energy to the mucosal epithelium (as well as reduced capacity for repair), and that this mechanism may be key in linking altered host−microbiome interactions to the pathogenesis of IBS.

The relationship between fatty liver and insulin resistance: a mystery to solve

Lyu K, Zhang Y, Zhang D, et al. A Membrane-Bound Diacylglycerol Species Induces PKCϵ-Mediated Hepatic Insulin Resistance. Cell Metab 2020; S1550-4131(20)30414–9. doi: 10.1016/j.cmet.2020.08.001.

Hepatic steatosis is …

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Footnotes

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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