Interleukin-6 and insulin resistance.
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.
Kim
Jeong-Ho
JH
Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
Bachmann
Rebecca A
RA
Chen
Jie
J
D000273:Adipose Tissue / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007249:Inflammation; D007333:Insulin Resistance / Q000502:physiology*; D015850:Interleukin-6 / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology
D015850:Interleukin-6; D005947:Glucose