Abstract

AbstractThiamine (vitamin B1) has a key role in protection against renal disease by providing the thiamine pyrophosphate cofactor for transketolase and thereby maintaining oxidative and reductive pentosephosphate pathway activities key in countering oxidative and metabolic stress. The link to renal disease is amplified by increased washout and deficiency in renal disease, which in diabetic nephropathy may be linked to tissue-specific downregulation of thiamine transporters. Transketolase is part of the antistress gene response coordinated by transcription factor NF-E2–related factor-2 (nrf2) and activated by dietary bioactive and synthetic activators. Such activators have been found to be beneficial in the treatment of diabetic nephropathy wherein increased transketolase activity may have a key role. High dose thiamine supplements prevented the development of nephropathy in experimental diabetes and in a recent pilot scale trial reversed early stage nephropathy in patients with type 2 diabetes. Transketolase gene TKT variability and increased fractional excretion of thiamine were linked to susceptibility and progression of diabetic nephropathy. A definitive, large-scale trial of thiamine supplements for treatment of early stage diabetic nephropathy is now desirable.KeywordsThiamineTransketolaseDiabetic nephropathyNF-E2-related factor-2 (nrf2)Diabetic nephropathy

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