Obesity Comorbidity/Etiology and Pathophysiology

Mechanisms linking obesity, inflammation and altered metabolism to colon carcinogenesis

  1. E. Yehuda-Shnaidman,
  2. B. Schwartz*

Article first published online: 3 SEP 2012

DOI: 10.1111/j.1467-789X.2012.01024.x

Issue

Obesity Reviews

Obesity Reviews

Volume 13, Issue 12, pages 1083–1095, December 2012

Additional Information

How to Cite

Yehuda-Shnaidman, E. and Schwartz, B. (2012), Mechanisms linking obesity, inflammation and altered metabolism to colon carcinogenesis. Obesity Reviews, 13: 1083–1095. doi: 10.1111/j.1467-789X.2012.01024.x

Author Information

  1. Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot, Israel

*Professor B Schwartz, Institute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, PO Box 12, Rehovot 76100, Israel. E-mail: bschwart@agri.huji.ac.il

Publication History

  1. Issue published online: 5 NOV 2012
  2. Article first published online: 3 SEP 2012
  3. Received 19 April 2012; revised 23 July 2012; accepted 23 July 2012

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Keywords:

  • Adipokines;
  • inflammatory colon cancer;
  • inflammation;
  • obesity

Summary

Due to its prevalence, obesity is now considered a global epidemic. It is linked to increased risk of colorectal cancer, the third most common cancer and the second leading cause of death among adults in Western countries. Obese adipose tissue differs from lean adipose tissue in its immunogenic profile, body fat distribution and metabolic profile. Obese adipose tissue releases free fatty acids, adipokines and many pro-inflammatory chemokines. These factors are known to play a key role in regulating malignant transformation and cancer progression. Obese adipose tissue is infiltrated by macrophages that participate in inflammatory pathways activated within the tissue. Adipose tissue macrophages consist of two different phenotypes. M1 macrophages reside in obese adipose tissue and produce pro-inflammatory cytokines, and M2 macrophages reside in lean adipose tissue and produce anti-inflammatory cytokines, such as interleukin-10 (IL-10). The metabolic networks that confer tumour cells with their oncogenic properties, such as increased proliferation and the ability to avoid apoptosis are still not well understood. We review the interactions between adipocytes and immune cells that may alter the metabolism towards promotion of colorectal cancer.

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