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The relevance of intestinal barrier dysfunction, antimicrobial proteins and bacterial endotoxin in metabolic dysfunction-associated steatotic liver disease.
Bergheim, Ina; Moreno-Navarrete, José María.
Afiliação
  • Bergheim I; Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Vienna, Austria.
  • Moreno-Navarrete JM; Nutrition, Eumetabolism and Health Group, Institut d'Investigació Biomèdica de Girona (IDIBGI-CERCA), Girona, Spain.
Eur J Clin Invest ; 54(7): e14224, 2024 Jul.
Article em En | MEDLINE | ID: mdl-38634717
ABSTRACT

BACKGROUND:

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of end-stage liver disease associated with increased mortality and cardiovascular disease. Obesity and diabetes are the most important risk factors of MASLD. It is well-established that obesity-associated insulin resistance leads to a situation of tissue lipotoxicity characterized by an accumulation of excess fat in non-fat tissues such as the liver, promoting the development of MASLD, and its progression into metabolic dysfunction-associated steatohepatitis.

METHODS:

Here, we aimed to review the impact of disrupted intestinal permeability, antimicrobial proteins and bacterial endotoxin in the development and progression of MASLD. RESULTS AND

CONCLUSION:

Recent studies demonstrated that obesity- and obesogenic diets-associated alterations of intestinal microbiota along with the disruption of intestinal barrier integrity, the alteration in antimicrobial proteins and, in consequence, an enhanced translocation of bacterial endotoxin into bloodstream might contribute to this pathological process through to impacting liver metabolism and inflammation.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Endotoxinas / Microbioma Gastrointestinal / Obesidade Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Endotoxinas / Microbioma Gastrointestinal / Obesidade Idioma: En Ano de publicação: 2024 Tipo de documento: Article