@inbook{f115d4774d614ef9a580afa05296fe86,
title = "Chapter 21 Interleukin-6 and Insulin Resistance",
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.",
keywords = "Adipose, Chronic inflammation, GLUT4, IL-6, Liver, SOCS, STAT, Skeletal muscle, insulin resistance",
author = "Kim, {Jeong Ho} and Bachmann, {Rebecca A.} and Jie Chen",
note = "Funding Information: Work from the authors{\textquoteright} laboratory was supported by funding from the National Institute of Health and the American Diabetes Association.",
year = "2009",
doi = "10.1016/S0083-6729(08)00621-3",
language = "English (US)",
isbn = "9780123744081",
series = "Vitamins and Hormones",
number = "C",
pages = "613--633",
booktitle = "Vitamins and Hormones",
edition = "C",
}