Sci. Aging Knowl. Environ., 12 March 2003
Vol. 2003, Issue 10, p. pe6
[DOI: 10.1126/sageke.2003.10.pe6]


Vitamin B1 Blocks Damage Caused by Hyperglycemia

Mark E. Obrenovich, and Vincent M. Monnier

The authors are in the Department of Pathology at Case Western Reserve University, Cleveland, OH 44106, USA. E-mail: vmm3{at} (V.M.M.);2003/10/pe6

Key Words: vitamin B1 • thiamine • diabetes • retinopathy • reactive oxygen species

Abstract: Diabetes accelerates the aging process and leads to complications that include blindness, renal failure, nerve damage, stroke, and cardiovascular disease. It has been hypothesized that high plasma glucose concentrations are responsible for increased mitochondrial free radical production and subsequent inactivation of glyceraldehyde phosphate dehydrogenase (GAPDH) in vascular endothelial cells and other cells implicated in these complications. As a result of the decreased ability of GAPDH to process upstream metabolites, three pathways of metabolic damage are activated, which include the advanced glycation end-product formation pathway, the protein kinase C pathway, and the hexosamine pathway. All three pathways have been implicated in abnormal cell signaling in diabetes. A group of German and U.S. scientists has now found that treating diabetic rats with high doses of benfotiamine, a lipid-soluble form of vitamin B1, can prevent diabetic retinopathy and all three forms of metabolic damage by stimulating transketolase activity and thus diverting excess metabolites toward the pentose pathway. Although vitamin B1 is available over the counter, the researchers at this time do not advocate self-treatment without further clinical data.

Citation: M. E. Obrenovich, V. M. Monnier, Vitamin B1 Blocks Damage Caused by Hyperglycemia. Sci. SAGE KE 2003, pe6 (12 March 2003);2003/10/pe6

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