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The pathogenic mechanism of insulin resistance and associated diseases such as metabolic syndrome and diabetes remains unclear. Since inflammatory cytokines secreted by T cells play an important role in immune system homeostasis, we evaluated the role of interleukin-6 (IL-6) and the Th17/Treg balance in insulin sensitivity and the underlying mechanism in a rat model. After establishing an insulin-resistant rat model, the rats were injected with anti-mouse IL-6R receptor antibody (MR16-1) to block IL-6. Adipose tissue and blood samples were obtained for the analysis of cytokines, Th17 and Treg markers, and insulin sensitivity blood parameters, for comparisons with those of the normal control group, IL-6-blocked control group, and insulin resistance control group. In the insulin resistance control group, the expression levels of IL-6, RORγt, and IL-17 increased, whereas those of IL-10, FoxP3, and CD4+CD25+Treg decreased. Insulin sensitivity decreased, whereas glucose, total serum cholesterol, triglycerides, and free fatty acid levels significantly increased. However, the completely opposite effects for all parameters were detected in the insulin resistance IL-6-blocked group. Insulin resistance can cause inflammation and an imbalance in Th17 cells/Treg cells. IL-6 can restore this imbalance and play an important role in the development and progression of insulin resistance.

Role and mechanism of the Th17/Treg cell balance in the development and progression of insulin resistance