Possible Metabolic Remodeling based on de novo Biosynthesis of L-serine in Se-Subtoxic or -Deficient Mammals.

Abstract

Current research studies point to an increased risk of diabetes with selenium (Se) intake beyond the physiological requirement used to prevent cancers. The existing hypothesis of "selenoprotein overexpression leads to intracellular redox imbalance" cannot clearly explain the U-shaped dose-effect relationship between Se intake and the risk of diabetes. In this review, it is speculated that metabolic remodeling based on the de novo biosynthesis of L-serine may occur in mammals at supranutritional or subtoxic levels of Se. It is also speculated that a large amount of L-serine is consumed by the body during insufficient Se intake, thus resulting in similar metabolic reprogramming. The increase in atypical ceramide and its derivatives due to the lack of L-serine may also play a role in the development of diabetes.