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Interleukin-6 and Diabetes

The Good, the Bad, or the Indifferent?

¹ Steno Diabetes Center, Gentofte, Denmark
² Department of Gastroenterology, Hvidovre Hospital, Hvidovre, Denmark
³ Department of Molecular Medicine, Karolinska Institute, Stockholm, Sweden

Inflammatory mechanisms play a key role in the pathogenesis of type 1 diabetes. Individuals who progress to type 2 diabetes display features of low-grade inflammation years in advance of disease onset. This low-grade inflammation has been proposed to be involved in the pathogenetic processes causing type 2 diabetes. Mediators of inflammation such as tumor necrosis factor-, interleukin (IL)-1ß, the IL-6 family of cytokines, IL-18, and certain chemokines have been proposed to be involved in the events causing both forms of diabetes. IL-6 has in addition to its immunoregulatory actions been proposed to affect glucose homeostasis and metabolism directly and indirectly by action on skeletal muscle cells, adipocytes, hepatocytes, pancreatic ß-cells, and neuroendocrine cells. Here we argue that IL-6 action—in part regulated by variance in the IL-6 and IL-6 receptor genes—contributes to, but is probably neither necessary nor sufficient for, the development of both type 1 and type 2 diabetes. Thus, the two types of diabetes are also in this respect less apart than apparent. However, the mechanisms are not clear, and we therefore propose future directions for studies in this field.

Abbreviations: CNS, central nervous system; ERK, extracellular signal-regulated kinase; IL, interleukin; IRS, insulin receptor substrate; JAK, Janus kinase; PMA, phorbol myristate acetate; SHP-2, Src homology 2–containing tyrosine phosphatase; SNP, single nucleotide polymorphism; SOCS, suppressors of cytokine signaling; STAT, signal transducers and activator of transcription

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