Abstract
Obesity-induced insulin resistance (IR) is associated with chronic low-grade inflammation. Elevated free fatty acids (FFA), as seen in obesity, can act as damage associated molecular patterns (DAMPs) to activate certain receptors of the innate immune system. We have previously shown that the nucleotide oligomerization domain (NOD) 1 receptor can be activated by saturated FFA in vitro and in vivo. NOD1 signals through an inflammatory kinase, RIPK2, which can lead to increased cytokine production.
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