The role of the gastrointestinal barrier in obesity-associated systemic inflammation

Obes Rev. 2024 Mar;25(3):e13673. doi: 10.1111/obr.13673. Epub 2023 Dec 18.

Abstract

Systemic inflammation is a key contributor to the onset and progression of several obesity-associated diseases and is thought to predominantly arise from the hyperplasia and hypertrophy of white adipose tissue. However, a growing body of works suggests that early changes in the gastrointestinal (GI) barrier may contribute to both local, within the GI lining, and systemic inflammation in obesity. Intestinal barrier dysfunction is well-characterized in inflammatory GI disorders such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) and is known to contribute to systemic inflammation. Thus, drawing parallels between GI disorders, where intestinal permeability and systemic inflammation are prominent features, and obesity-induced GI manifestations may provide insights into the potential role of the intestinal barrier in systemic inflammation in obesity. This review summarizes the current literature surrounding intestinal barrier dysfunction in obesity and explores the potential role of intestinal hyperpermeability and intestinal barrier dysfunction in the development of systemic inflammation and GI dysfunction in obesity.

Keywords: enteric neurons; gastrointestinal dysfunction; leaky gut; obesity; systemic inflammation.

Publication types

  • Review

MeSH terms

  • Gastrointestinal Tract*
  • Humans
  • Inflammation / etiology
  • Intestinal Mucosa*
  • Intestines
  • Obesity / complications