Wang Jianrong, Zhang Xue, Zhan Shuo, Han Feng, Wang Qin, Liu Yiqun, Huang Zhenwu
Department of Nutrition and Metabolism, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing, PR China.
Department of Nutrition and Metabolism, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing, PR China.
J Nutr. 2025 Jan;155(1):9-26. doi: 10.1016/j.tjnut.2024.10.041. Epub 2024 Oct 28.
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.
当前的研究表明，当硒（Se）摄入量超过用于预防癌症的生理需求量时，患糖尿病的风险会增加。现有的“硒蛋白过表达导致细胞内氧化还原失衡”假说无法清楚地解释硒摄入量与糖尿病风险之间的U型剂量效应关系。在本综述中，推测在超营养或亚毒性水平的硒作用下，哺乳动物体内可能会发生基于L-丝氨酸从头生物合成的代谢重塑。还推测在硒摄入不足时，身体会消耗大量L-丝氨酸，从而导致类似的代谢重编程。由于缺乏L-丝氨酸导致的非典型神经酰胺及其衍生物的增加，也可能在糖尿病的发展中起作用。
