Editorial
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2025; 31(1): 102042
Published online Jan 7, 2025. doi: 10.3748/wjg.v31.i1.102042
Creeping fat and gut microbiota in Crohn’s disease
Ana EV Quaglio, Daniéla O Magro, Marcello Imbrizi, Ellen CS De Oliveira, Luiz C Di Stasi, Ligia Y Sassaki
Ana EV Quaglio, Verum Ingredients, Botucatu Technology Park, Botucatu 18605-525, São Paulo, Brazil
Daniéla O Magro, Department of Surgery, Faculty of Medical Sciences, State University of Campinas, Campinas 13083-970, São Paulo, Brazil
Marcello Imbrizi, Department of Gastroenterology, Faculty of Medical Sciences, University of Campinas, Campinas 13083-970, São Paulo, Brazil
Ellen CS De Oliveira, Ligia Y Sassaki, Department of Internal Medicine, Medical School, São Paulo State University, Botucatu 18618-686, São Paulo, Brazil
Luiz C Di Stasi, Department of Biophysics and Pharmacology, Institute of Biosciences, São Paulo State University, Botucatu 18618-689, São Paulo, Brazil
Author contributions: Quaglio AEV, Magro DO, Imbrizi M, De Oliveira ECS, Di Stasi LC, and Sassaki LY contributed equally to the conception and design of the article, writing, and editing of the manuscript, and review of the literature; All the authors approved the final version of the article to be published.
Supported by the Postdoctoral Scholarship Grant, No. 5552/2024 PROPG/PROPE N°06/2024.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ligia Y Sassaki, MD, PhD, Professor, Research Associate, Department of Internal Medicine, Medical School, São Paulo State University, Av. Prof. Montenegro-Distrito de, Botucatu-SP, Botucatu 18618-686, São Paulo, Brazil. ligia.sassaki@unesp.br
Received: October 7, 2024
Revised: November 1, 2024
Accepted: November 13, 2024
Published online: January 7, 2025
Processing time: 62 Days and 14.6 Hours
Abstract

In this article, we explored the role of adipose tissue, especially mesenteric adipose tissue and creeping fat, and its association with the gut microbiota in the pathophysiology and progression of Crohn’s disease (CD). CD is a form of inflammatory bowel disease characterized by chronic inflammation of the gastrointestinal tract, influenced by genetic predisposition, gut microbiota dysbiosis, and environmental factors. Gut microbiota plays a crucial role in modulating immune response and intestinal inflammation and is associated with the onset and progression of CD. Further, visceral adipose tissue, particularly creeping fat, a mesenteric adipose tissue characterized by hypertrophy and fibrosis, has been implicated in CD pathogenesis, inflammation, and fibrosis. The bacteria from the gut microbiota may translocate into mesenteric adipose tissue, contributing to the formation of creeping fat and influencing CD progression. Although creeping fat may be a protective barrier against bacterial invasion, its expansion can damage adjacent tissues, leading to complications. Modulating gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and prebiotics has shown potential in managing CD. However, more research is needed to clarify the mechanisms linking gut dysbiosis, creeping fat, and CD progression and develop targeted therapies for microbiota modulation and fat-related complications in patients with CD.

Keywords: Creeping fat; Mesenteric adipose tissue; Gut microbiota; Crohn’s disease; Inflammatory bowel disease

Core Tip: Crohn’s disease is associated with creeping fat accumulation, influenced by factors such as gut microbiota. Dysbiosis, characterized by an increase in proteobacteria and species such as Clostridium innocuum, contributes to mesenteric fat accumulation and exacerbates inflammation. Modulating the microbiota through individualized interventions, such as environmental exposure modifications, fecal microbiota transplantation, and probiotics and prebiotics use, may be a potential strategy to reduce intestinal inflammation and mesenteric fat proliferation, improving therapeutic outcomes. However, further research is needed to elucidate the molecular mechanisms involved and develop biomarkers to identify patients who would benefit most from these approaches, considering their individual characteristics.