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Interleukin-1 (IL-1) can activate nuclear factor-B (NF-B) signal pathway and cause islet cell dysfunction, which leads to hyperglycemia

The interactions between citrulline and molecules associated with the JAK/STAT axis, together with the regulatory effects of urea cycle-related enzymes on the activation of inflammatory macrophages, suggest that the iNOS/NO axis may exert feedback regulation on pro-inflammatory signaling in different contexts ( At the intervention level, regulating the metabolic partitioning of Arg can alter macrophage phenotypes and inflammatory intensity

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1 This fact makes ASCT1, ASCT2 and EAAT3 pivotal in the reliance of cancer cells on cysteine uptake and anabolism