How the association between obesity and inflammation may lead to insulin resistance and cancer

Diabetes Metab Syndr. Mar-Apr 2019;13(2):1213-1224. doi: 10.1016/j.dsx.2019.01.041. Epub 2019 Jan 29.


Background and objectives: Obesity is associated with metabolic dysfunction and over nutrition. Increased body mass index and obesity are strongly amalgamated with changes in the physiological function of adipose tissue, leading to altered secretion of adipocytokines, inflammatory mediators release as well as chronic inflammation and insulin resistance. The purposes of this study were to review the evidence of how obesity and inflammation may lead to insulin resistance and cancer.

Summary: Recent findings suggested that increased level of inflammatory mediators in obesity, plays an introductory and cabalistic role in the development of different types of inflammatory disorders including type 2 diabetes mellitus. Link between elevated body mass index and type 2 diabetes mellitus (T2DM). Several of the factors-such as increased levels of leptin, plasminogen activator inhibitor-1, decreased levels of adiponectin, insulin resistance, chronic inflammation etc. consequently result in carcinogenesis and carcinogenic progression too.

Conclusion: This review summarizes how cytokine production in adipose tissue of obese subject creates a chronic inflammatory environment that favors tumor cell motility and invasion to enhance the metastatic potential of tumor cells. High levels of cytokine in the circulation of affected individuals have been associated with a significantly worse outcome. This article also reconnoiters the mechanisms that link obesity to numerous disorders such as inflammation, diabetes, cancers and most specifically combine these processes in a single image. Understanding these mechanisms may assist to understand the consequences of obesity.

Keywords: Adiposity; Cancer; Diabetes; Inflammation; Obesity.

Publication types

  • Review

MeSH terms

  • Humans
  • Inflammation / complications*
  • Insulin Resistance*
  • Neoplasms / etiology*
  • Neoplasms / pathology
  • Obesity / complications*
  • Prognosis