Animal studies have shown that inflammation caused by type 2 diabetes leads to inflammation-related expression profiles in the superior cervical ganglion and SG, including co-expression of mRNAs related to immune response and chemokines (31), as well as the asynchronous release of neurotransmitters of tyrosine hydroxylase (TH), exacerbating sympathetic nerve dysregulation (32). This evidence concerns the gene TH and type 2 diabetes mellitus.