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1 Introduction The pathogenesis of autoimmune type 1 diabetes mellitus (T1D) involves infiltration of the pancreatic islet cells by T-lymphocytes, macrophages, and other immune cells with consequent loss of insulin producing -cells ( Outside of the CNS, GABA is highly concentrated in the pancreatic islet wherein it has autocrine and paracrine actions to regulate -cell insulin secretion and inhibit -cell glucagon release

Mass spectrometry analysis of the GSSG-treated sample indeed confirmed that the CCLC motif can harbour one intramolecular disulfide plus one glutathionylated cysteine at the same time (Fig