Chapter 21 Interleukin-6 and Insulin Resistance

Jeong Ho Kim, Rebecca A. Bachmann, Jie Chen

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Chronic low-grade inflammation has been well recognized as a key feature of obesity that is correlated with insulin resistance and type 2 diabetes. Among the adipose-secreted factors (adipokines), the inflammatory regulator interleukin-6 (IL-6) has emerged as one of the potential mediators that link obesity-derived chronic inflammation with insulin resistance. Adipose tissue contributes to up to 35% of circulating IL-6, the systemic effects of which have been best demonstrated in the liver, where a STAT3-SOCS-3 pathway mediates IL-6 impairment of insulin actions. However, this cytokine displays pleiotropic functions in a tissue-specific and physiological context-dependent manner. In contrast to its role in liver, IL-6 is believed to be beneficial for insulin-regulated glucose metabolism in muscle. Furthermore, the effects of the cytokine are seemingly influenced by whether it is present acutely or chronically; the latter is the setting associated with insulin resistance. Herein we review the in vivo and in vitro studies that have examined the role of IL-6 in insulin signaling and glucose metabolism in the insulin target tissues: liver, adipose, and skeletal muscle.

Original languageEnglish (US)
Title of host publicationVitamins and Hormones
Pages613-633
Number of pages21
EditionC
DOIs
StatePublished - Mar 5 2009

Publication series

NameVitamins and Hormones
NumberC
Volume80
ISSN (Print)0083-6729

Keywords

  • Adipose
  • Chronic inflammation
  • GLUT4
  • IL-6
  • Liver
  • SOCS
  • STAT
  • Skeletal muscle
  • insulin resistance

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

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