Obesity, Bioactive Lipids, and Adipose Tissue Inflammation in Insulin Resistance

Nutrients. 2020 May 3;12(5):1305. doi: 10.3390/nu12051305.


Obesity is a major risk factor for the development of insulin resistance and type 2 diabetes. The exact mechanism by which adipose tissue induces insulin resistance is still unclear. It has been demonstrated that obesity is associated with the adipocyte dysfunction, macrophage infiltration, and low-grade inflammation, which probably contributes to the induction of insulin resistance. Adipose tissue synthesizes and secretes numerous bioactive molecules, namely adipokines and cytokines, which affect the metabolism of both lipids and glucose. Disorders in the synthesis of adipokines and cytokines that occur in obesity lead to changes in lipid and carbohydrates metabolism and, as a consequence, may lead to insulin resistance and type 2 diabetes. Obesity is also associated with the accumulation of lipids. A special group of lipids that are able to regulate the activity of intracellular enzymes are biologically active lipids: long-chain acyl-CoAs, ceramides, and diacylglycerols. According to the latest data, the accumulation of these lipids in adipocytes is probably related to the development of insulin resistance. Recent studies indicate that the accumulation of biologically active lipids in adipose tissue may regulate the synthesis/secretion of adipokines and proinflammatory cytokines. Although studies have revealed that inflammation caused by excessive fat accumulation and abnormalities in lipid metabolism can contribute to the development of obesity-related insulin resistance, further research is needed to determine the exact mechanism by which obesity-related insulin resistance is induced.

Keywords: adipokines; adipose tissue; biologically active lipids; cytokines; insulin resistance; obesity.

Publication types

  • Review

MeSH terms

  • Adipokines / metabolism
  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology*
  • Cytokines / metabolism
  • Diabetes Mellitus, Type 2 / etiology*
  • Diabetes Mellitus, Type 2 / metabolism
  • Glucose / metabolism
  • Humans
  • Inflammation / etiology
  • Inflammation Mediators / metabolism
  • Insulin Resistance / physiology*
  • Lipid Metabolism / physiology*
  • Macrophages / pathology
  • Obesity / complications
  • Obesity / metabolism*
  • Obesity / pathology*
  • Risk Factors


  • Adipokines
  • Cytokines
  • Inflammation Mediators
  • Glucose