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World J Meta-Anal. Mar 18, 2026; 14(1): 113789
Published online Mar 18, 2026. doi: 10.13105/wjma.v14.i1.113789
Metabolic dysfunction-associated fatty liver disease: A key player in colorectal cancer development and progression
Yasser Fouad, Ziyan Pan, Alaa M Mostafa, Mohammed Eslam
Yasser Fouad, Alaa M Mostafa, Department of Gastroenterology, Hepatology and Endemic Medicine, Faculty of Medicine, Minia University, Minia 19111, Egypt
Ziyan Pan, Mohammed Eslam, Storr Liver Centre, Westmead Institute for Medical Research, Westmead Hospital and University of Sydney, Sydney 2145, Australia
Author contributions: Fouad Y and Eslam M designed the work; Mostafa AM and Pan Z collected the data; Fouad Y, Pan Z, Mostafa AM, and Eslam M contributed to writing the draft; All authors thoroughly reviewed and endorsed the final manuscript.
Conflict-of-interest statement: All authors report no relevant conflicts of interest for this article.
Corresponding author: Yasser Fouad, MD, Professor, Department of Gastroenterology, Hepatology and Endemic Medicine, Faculty of Medicine, Minia University, El-Horria Street, Minia 19111, Egypt. yasser.abdallah@mu.edu.eg
Received: September 5, 2025
Revised: October 9, 2025
Accepted: December 11, 2025
Published online: March 18, 2026
Processing time: 187 Days and 1.8 Hours
Abstract

Metabolic dysfunction-associated fatty liver disease (MAFLD) may actively contribute to the development, progression, and outcomes of colorectal cancer (CRC) in addition to coexisting with it, according to mounting epidemiological and mechanistic evidence. Obesity, type 2 diabetes, dietary patterns, and systemic inflammation are among the risk factors that overlap between the two conditions, indicating a convergent pathophysiological axis. Insulin resistance, altered adipokine signaling, gut microbiota dysbiosis, chronic low-grade inflammation, and hepatic fibrogenesis are key mechanisms that connect MAFLD and CRC. Together, these pathways foster an environment that is protumorigenic and marked by immunological dysregulation, oxidative stress, and lipotoxicity. Comprehending this reciprocal relationship presents a special chance for integrated management and prevention tactics. Changing one’s lifestyle, controlling metabolic risk factors, and using new therapeutic targets like anti-inflammatory and antifibrotic drugs may help slow the progression of MAFLD and lower the burden of CRC. In addition to calling for future research to define customized interventions that can simultaneously mitigate the burden of both MAFLD and CRC, this perspective emphasized the necessity of multidisciplinary strategies aimed at prevention, early detection, and therapeutic optimization.

Keywords: Metabolic associated fatty liver disease; Colorectal carcinoma; Risk factors; Colon; Liver

Core Tip: Metabolic dysfunction-associated fatty liver disease may actively contribute to the development, progression, and outcomes of colorectal cancer in addition to coexisting with it, according to mounting epidemiological and mechanistic evidence. Obesity, type 2 diabetes, dietary patterns, and systemic inflammation are among the risk factors that overlap between the two conditions, indicating a convergent pathophysiological axis. Changing one’s lifestyle, controlling metabolic risk factors, and using new therapeutic targets like anti-inflammatory and antifibrotic drugs may help slow the progression of metabolic dysfunction-associated fatty liver disease and lower the burden of colorectal cancer. This perspective emphasized the necessity of multidisciplinary strategies aimed at prevention, early detection, and therapeutic optimization.