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Med Hypotheses. 2012 Jan;78(1):179-82. doi: 10.1016/j.mehy.2011.10.021. Epub 2011 Nov 15.

Pyridoxal 5'-phosphate (PLP) deficiency might contribute to the onset of type I diabetes.

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Department of Experimental and Health Sciences (DCEXS), Pompeu Fabra University, PRBB-Barcelona Biomedical Research Park, c/ Dr. Aiguader, 88 E-08003 Barcelona, Spain.


The incidence of type I diabetes is rising worldwide, particularly in young children. Type I diabetes is considered a multifactorial disease with genetic predisposition and environmental factors participating. Currently, despite years of research, there is no consensus regarding the factors that initiate the autoimmune response. Type I diabetes is preceded by autoimmunity to islet antigens, among them the protein glutamic acid decarboxylase, GAD-65. Pyridoxal 5'-phosphate (PLP) is formed from vitamin B6 by the action of pyridoxal kinase. Interaction of GAD65 with PLP is necessary for GAD65-mediated synthesis of the neurotransmitter γ-aminobutyric acid (GABA). PLP is also a required cofactor for dopamine synthesis by L-aromatic decarboxylase (L-AADC). Both GAD65 and L-AADC are expressed in pancreatic islets. Here it is proposed that lack of the vitamin B6 derivative pyridoxal 5'-phosphate might contribute to the appearance of pancreatic islet autoimmunity and type I diabetes onset.

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