Autor: |
Maroulla D. Nikolaki, Arezina N. Kasti, Konstantinos Katsas, Konstantinos Petsis, Sophia Lambrinou, Vasiliki Patsalidou, Sophia Stamatopoulou, Katerina Karlatira, John Kapolos, Konstantinos Papadimitriou, Konstantinos Triantafyllou |
Jazyk: |
angličtina |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
Microorganisms, Vol 11, Iss 10, p 2387 (2023) |
Druh dokumentu: |
article |
ISSN: |
2076-2607 |
DOI: |
10.3390/microorganisms11102387 |
Popis: |
The literature about the association of branched short-chain fatty acids (BCFAs) and irritable bowel syndrome (IBS) is limited. BCFAs, the bacterial products of the catabolism of branched-chain amino acids, are proposed as markers for colonic protein fermentation. IBS is a gastrointestinal disorder characterized by low-grade inflammation and intestinal dysbiosis. The low-FODMAP diet (LFD) has increasingly been applied as first-line therapy for managing IBS symptoms, although it decreases the production of short-chain fatty acids (SCFA), well known for their anti-inflammatory action. In parallel, high protein consumption increases BCFAs. Protein fermentation alters the colonic microbiome through nitrogenous metabolites production, known for their detrimental effects on the intestinal barrier promoting inflammation. Purpose: This review aims to explore the role of BCFAs on gut inflammation in patients with IBS and the impact of LFD in BCFAs production. Methods: A literature search was carried out using a combination of terms in scientific databases. Results: The included studies have contradictory findings about how BCFAs affect the intestinal health of IBS patients. Conclusions: Although evidence suggests that BCFAs may play a protective role in gut inflammation, other metabolites of protein fermentation are associated with gut inflammation. Further research is needed in order to clarify how diet protein composition and, consequently, the BCFAs are implicated in IBS pathogenesis or in symptoms management with LFD+. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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