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Insulin resistance (IR) has long been considered as a major hallmark for the etiology and pathogenesis of type 2 diabetes mellitus (T2DM). Development of IR is mainly associated with low-grade tissue-specific inflammatory responses induced by various pro-inflammatory and/or oxidative stress mediators notably pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6.

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At the molecular level, two underlying mechanisms of insulin resistance have been proposed, both involving defective insulin signal transduction [52, 62,63]. The first mechanism describes.

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