4.7 Review

The metabolic nature of inflammatory bowel diseases

期刊

NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
卷 19, 期 12, 页码 753-767

出版社

NATURE PORTFOLIO
DOI: 10.1038/s41575-022-00658-y

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资金

  1. Austrian Science Fund [FWF P33070]
  2. European Research Council [ERC-STG: 101039320]
  3. Austrian Society of Gastroenterology & Hepatology (oGGH)
  4. Tyrolean Science Funds (TWF)
  5. excellence initiative (Competence Centers for Excellent Technologies - COMET) of the Austrian Research Promotion Agency FFG: Research Center of Excellence in Vascular Ageing Tyrol, VASCage - BMVIT [843536]
  6. excellence initiative (Competence Centers for Excellent Technologies - COMET) of the Austrian Research Promotion Agency FFG: Research Center of Excellence in Vascular Ageing Tyrol, VASCage - BMWFW [843536]
  7. excellence initiative (Competence Centers for Excellent Technologies - COMET) of the Austrian Research Promotion Agency FFG: Research Center of Excellence in Vascular Ageing Tyrol, VASCage - Wirtschaftsagentur Wien [843536]
  8. excellence initiative (Competence Centers for Excellent Technologies - COMET) of the Austrian Research Promotion Agency FFG: Research Center of Excellence in Vascular Ageing Tyrol, VASCage - Standortagentur Tirol [843536]

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Experimental and clinical evidence support the role of metabolic perturbation in gut inflammation in IBD, which is linked to dietary factors. These studies also highlight the connection between metabolism and inflammation in IBD.
Experimental and clinical evidence supports a role of metabolic perturbation in the development of gut inflammation in inflammatory bowel disease (IBD). This Review discusses the role of diet and metabolic inflammation in IBD, outlining key concepts and highlighting the links between metabolism and inflammation in IBD. Crohn's disease and ulcerative colitis, phenotypically comprising a spectrum of inflammatory bowel diseases (IBDs), spread globally during the westernization of lifestyle and dietary habits over the past few decades. Here, we review experimental and clinical evidence for the metabolic nature of gut inflammation in IBD and delineate distinct parallels to the inflammatory state in metabolic diseases. Experimental evidence indicates that excessive intake of specific macronutrients in a Western diet fuels an inflammatory response in the gut by exploiting sensors of innate immunity and perturbation of gut microbial metabolism. Genetic IBD risk partly affects metabolism and stress signalling of innate immunity, and immunometabolism controls susceptibility to gut inflammation. Epidemiological and clinical studies indicate that specific nutrients in the Western diet pose a risk for the development of IBD and a poor disease course. Translational studies in IBD indicate perturbation of energy metabolism in immune cells and perturbation of gut microbial metabolism, which can be shaped by diet. In turn, dietary restriction by exclusive enteral nutrition induces remission in patients with IBD. Collectively, these studies support a metabolic underpinning of gut inflammation in IBD as described for metabolic inflammation in obesity and related disorders.

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