Inflammation and endoplasmic reticulum stress in obesity and diabetes

Int J Obes (Lond). 2008 Dec;32 Suppl 7(Suppl 7):S52-4. doi: 10.1038/ijo.2008.238.


Obesity is associated with chronic low-grade inflammation. Inflammatory signals interfere with insulin action and disrupt metabolic homeostasis. The c-Jun N-terminal kinase (JNK) has been identified as a central mediator of insulin resistance. Recent studies showed that in obesity compromising endoplasmic reticulum (ER) function results in insulin resistance and type 2 diabetes that are dependent on JNK activation. In contrast, enhancing ER function in transgenic mice or by the use of chemical chaperones protects against diet-induced insulin resistance. Hence, ER stress and the related signaling networks present a critical mechanism underlying obesity-induced JNK activity, inflammatory response and insulin resistance.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue / enzymology
  • Animals
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Endoplasmic Reticulum / enzymology
  • Endoplasmic Reticulum / physiology*
  • Humans
  • Inflammation / physiopathology*
  • Insulin Resistance / physiology*
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism*
  • Mice
  • Models, Biological
  • Obesity / physiopathology*
  • Protein Folding
  • Stress, Physiological


  • JNK Mitogen-Activated Protein Kinases