Gao F, Jiao Y, Wang HL. Metabolic syndrome and colorectal cancer: Mechanisms, epidemiological evidence, and clinical implications. World J Clin Oncol 2025; 16(12): 112639 [DOI: 10.5306/wjco.v16.i12.112639]
Corresponding Author of This Article
He-Lei Wang, Center of General Surgery, Department of Gastrointestinal Surgery, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun 130021, Jilin Province, China. helei@jlu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which 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: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Dec 24, 2025; 16(12): 112639 Published online Dec 24, 2025. doi: 10.5306/wjco.v16.i12.112639
Metabolic syndrome and colorectal cancer: Mechanisms, epidemiological evidence, and clinical implications
Fei Gao, Yan Jiao, He-Lei Wang
Fei Gao, The Anesthesia Recovery Room, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Yan Jiao, Center of General Surgery, Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
He-Lei Wang, Center of General Surgery, Department of Gastrointestinal Surgery, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China
Co-corresponding authors: Yan Jiao and He-Lei Wang.
Author contributions: Gao F wrote the initial draft, contributed to literature review; Jiao Y and Wang HL contributed to the study design; Jiao Y and Wang HL contributed equally to this manuscript and are co-corresponding authors. All authors approved the final version to be published.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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 NonCommercial (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: He-Lei Wang, Center of General Surgery, Department of Gastrointestinal Surgery, The First Hospital of Jilin University, No. 1 Xinmin Street, Changchun 130021, Jilin Province, China. helei@jlu.edu.cn
Received: August 4, 2025 Revised: September 4, 2025 Accepted: November 14, 2025 Published online: December 24, 2025 Processing time: 144 Days and 4.3 Hours
Abstract
Metabolic syndrome (MetS), characterized by central obesity, insulin resistance, dyslipidemia, and hypertension, has been increasingly recognized as a significant contributor to the development and progression of colorectal cancer (CRC). This review comprehensively summarizes current evidence linking MetS to CRC risk and outcomes from mechanistic, epidemiological, and clinical perspectives. Mechanistic studies suggest that hyperinsulinemia, activation of the insulin-like growth factor axis, chronic systemic inflammation, and adipokine dysregulation create a tumor-promoting environment. Epidemiological data from large-scale cohort studies and meta-analyses consistently demonstrate a positive association between MetS and CRC incidence, with abdominal obesity and hyperglycemia identified as key components. Mendelian randomization studies further support a causal relationship between visceral adiposity and CRC risk. Clinically, MetS is associated with increased risk of recurrence and reduced overall and disease-free survival in CRC patients. Emerging evidence also indicates that persistent metabolic abnormalities may contribute to early-onset CRC. Interventions targeting metabolic health - including lifestyle modification and bariatric surgery - have shown potential in reducing CRC risk and improving outcomes. Despite these advances, heterogeneity in MetS definitions and a paucity of prospective interventional studies limit the generalizability of current findings. Further research is warranted to establish standardized diagnostic criteria, elucidate sex- and age-specific mechanisms, and integrate metabolic profiling into risk stratification frameworks for CRC prevention and management.
Core Tip: This comprehensive review highlights the emerging role of metabolic syndrome (MetS) as a critical modifiable risk factor in colorectal cancer (CRC) initiation, progression, and prognosis. It synthesizes mechanistic evidence involving insulin resistance, chronic inflammation, and adipokine dysregulation, and consolidates global epidemiological data linking MetS - especially abdominal obesity and hyperglycemia - to increased CRC incidence and mortality. The review also discusses the adverse impact of MetS on CRC outcomes, including recurrence and survival, and evaluates the potential of lifestyle and surgical interventions in mitigating these risks. This article underscores the importance of integrating metabolic health assessment into personalized CRC prevention and management strategies.
