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Peer-reviewedCC BY-NC-ND 4.0In Vivo

The Interplay Between Obesity, Gut Microbiota and Early-onset Colorectal Cancer

  • SITI MARYAM AHMAD KENDONG1,2
  • NURUL NADIRAH RAZALI1
  • MYAT SU BO2
  • MARLYNNA SARKAWI2
  • MOHD HELMY MOKHTAR1
  • ADILA A. HAMID1
  1. 1Department of Physiology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia
  2. 2Department of Basic Medical Sciences, Faculty of Medicine and Health Sciences, Universiti Malaysia Sarawak, Sarawak, Malaysia
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Abstract

The global incidence of colorectal cancer (CRC) is rising at an alarming rate, particularly among individuals under the age of 50, referred to as early-onset CRC (EOCRC). While genetic predisposition accounts for approximately 20% of the total cases, the majority are influenced by environmental and lifestyle factors. Among these, the rising prevalence of obesity is a major modifiable contributor to EOCRC pathogenesis.This narrative review explores the multifaceted role of obesity in EOCRC, focusing on how diet-induced adiposity reshapes the gut microbiota and host metabolic signaling.We synthesize evidence on how obesity-associated dysbiosis, characterized by the depletion of protective, short-chain fatty acid (SCFA)-producing bacteria and the enrichment of genotoxic pathobionts, compromises intestinal barrier integrity and promotes a “leaky gut” phenotype. In addition, we explore the systemic consequences of obesity-driven inflammation, including M1-polarized macrophage infiltration into adipose tissue, dysregulated adipokine signaling, and the hyperactivation of the insulin-IGF-1 axis.By integrating epidemiological data with molecular mechanisms, this review highlights how the synergy between metabolic dysfunction and microbial alterations creates a fertile niche for early-onset carcinogenesis. These findings underscore the importance of targeting lifestyle interventions to mitigate the rising burden of obesity and reduce the risk of EOCRC progression.

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Cite

BibTeXRIS
BibTeX
@article{kendong2026interplay,
  title = {{The Interplay Between Obesity, Gut Microbiota and Early-onset Colorectal Cancer}},
  author = {SITI MARYAM AHMAD KENDONG and NURUL NADIRAH RAZALI and MYAT SU BO and MARLYNNA SARKAWI and MOHD HELMY MOKHTAR and ADILA A. HAMID},
  journal = {In Vivo},
  year = {2026},
  month = oct,
  doi = {10.21873/invivo.14478},
  url = {https://doi.org/10.21873/invivo.14478},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - The Interplay Between Obesity, Gut Microbiota and Early-onset Colorectal Cancer
AU  - SITI MARYAM AHMAD KENDONG
AU  - NURUL NADIRAH RAZALI
AU  - MYAT SU BO
AU  - MARLYNNA SARKAWI
AU  - MOHD HELMY MOKHTAR
AU  - ADILA A. HAMID
PY  - 2026
DA  - 2026/10/29
JO  - In Vivo
DO  - 10.21873/invivo.14478
UR  - https://doi.org/10.21873/invivo.14478
AB  - The global incidence of colorectal cancer (CRC) is rising at an alarming rate, particularly among individuals under the age of 50, referred to as early-onset CRC (EOCRC). While genetic predisposition accounts for approximately 20% of the total cases, the majority are influenced by environmental and lifestyle factors. Among these, the rising prevalence of obesity is a major modifiable contributor to EOCRC pathogenesis.This narrative review explores the multifaceted role of obesity in EOCRC, focusing on how diet-induced adiposity reshapes the gut microbiota and host metabolic signaling.We synthesize evidence on how obesity-associated dysbiosis, characterized by the depletion of protective, short-chain fatty acid (SCFA)-producing bacteria and the enrichment of genotoxic pathobionts, compromises intestinal barrier integrity and promotes a “leaky gut” phenotype. In addition, we explore the systemic consequences of obesity-driven inflammation, including M1-polarized macrophage infiltration into adipose tissue, dysregulated adipokine signaling, and the hyperactivation of the insulin-IGF-1 axis.By integrating epidemiological data with molecular mechanisms, this review highlights how the synergy between metabolic dysfunction and microbial alterations creates a fertile niche for early-onset carcinogenesis. These findings underscore the importance of targeting lifestyle interventions to mitigate the rising burden of obesity and reduce the risk of EOCRC progression.
SN  - 0258-851X
SN  - 1791-7549
ER  -