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The role of the thioredoxin/thioredoxin reductase system in the metabolic syndrome: towards a possible prognostic marker?
Authors:Alexey A Tinkov  Geir Bjørklund  Anatoly V Skalny  Margarita G Skalnaya  Salvatore Chirumbolo  Jan Aaseth
Institution:1.Yaroslavl State University,Yaroslavl,Russia;2.Peoples’ Friendship University of Russia (RUDN University),Moscow,Russia;3.Institute of Cellular and Intracellular Symbiosis,Russian Academy of Sciences,Orenburg,Russia;4.Council for Nutritional and Environmental Medicine,Mo i Rana,Norway;5.Trace Element Institute for UNESCO,Lyon,France;6.Orenburg State University,Orenburg,Russia;7.Department of Medical Biochemistry and Biophysics (MBB),Karolinska Institute,Stockholm,Sweden;8.Department of Neurological and Movement Sciences,University of Verona,Verona,Italy;9.Research Department,Innlandet Hospital Trust,Brumunddal,Norway;10.Inland Norway University of Applied Sciences,Elverum,Norway
Abstract:Mammalian thioredoxin reductase (TrxR) is a selenoprotein with three existing isoenzymes (TrxR1, TrxR2, and TrxR3), which is found primarily intracellularly but also in extracellular fluids. The main substrate thioredoxin (Trx) is similarly found (as Trx1 and Trx2) in various intracellular compartments, in blood plasma, and is the cell’s major disulfide reductase. Thioredoxin reductase is necessary as a NADPH-dependent reducing agent in biochemical reactions involving Trx. Genetic and environmental factors like selenium status influence the activity of TrxR. Research shows that the Trx/TrxR system plays a significant role in the physiology of the adipose tissue, in carbohydrate metabolism, insulin production and sensitivity, blood pressure regulation, inflammation, chemotactic activity of macrophages, and atherogenesis. Based on recent research, it has been reported that the modulation of the Trx/TrxR system may be considered as a new target in the management of the metabolic syndrome, insulin resistance, and type 2 diabetes, as well as in the treatment of hypertension and atherosclerosis. In this review evidence about a possible role of this system as a marker of the metabolic syndrome is reported.
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