CRP and Hyperglycemia: In this sense, it has been shown that hyperglycemia promotes the excessive formation of advanced glycation end products (AGEs), and these activate nuclear factor κB (NFκB), which triggers the transcription of pro-inflammatory cytokine promoter genes, and, in turn, the latter stimulate the production of CRP in the liver, which is why the protein is elevated in individuals with T2D [49,50], as was observed in the PG.