FABP4 and Insulin resistance: The treatment of human THP-1 macrophages with intermittent high glucose stimulated the expression of A-FABP, which subsequently mediated inflammatory cytokine (TNF-α and IL-1β) secretion through activating TLR4/p-JNK signaling cascade [50], which implicates the additional regulatory effect of A-FABP on inflammation in response to glucose fluctuation under insulin resistance.