Lin Shujing, Chen Chen, Ouyang Pei, Cai Zhiyu, Liu Xibei, Abdurahman Anwar, Peng Jiaying, Li Yu, Zhang Zhonghao, Song Guo-Li
Shenzhen Key Laboratory of Marine Bioresources and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong518060, People's Republic of China.
Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen, Guangdong518000, People's Republic of China.
J Agric Food Chem. 2023 Jan 25;71(3):1607-1619. doi: 10.1021/acs.jafc.2c07491. Epub 2023 Jan 12.
Selenium, a trace element associated with memory impairment and glucose metabolism, mainly exerts its function through selenoproteins. is a selenoprotein located in the endoplasmic reticulum (ER) lumen. Our study demonstrates for the first time that knockout decreases synaptic plasticity and causes memory impairment in 10-month-old mice. In addition, knockout causes hyperglycaemia and disturbs glucose metabolism, which is essential for synapse formation and transmission in the brain. Further research reveals that knockout leads to inhibition of the brain insulin signaling pathway [phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR/p70 S6 kinase pathway], which may impair synaptic plasticity in mice. High-fat diet (HFD) feeding suppresses the brain insulin signaling pathway in knockout mice and leads to earlier onset of cognitive impairment at 5 months of age. In general, our study demonstrates that knockout induces synaptic deficits via the brain insulin signaling pathway, thus leading to cognitive dysfunction in mice. These data strongly suggest that plays a vital role in brain glucose metabolism and contributes substantially to synaptic plasticity.
硒是一种与记忆障碍和葡萄糖代谢相关的微量元素，主要通过硒蛋白发挥其功能。[具体硒蛋白名称]是一种位于内质网（ER）腔中的硒蛋白。我们的研究首次表明，[硒蛋白名称]基因敲除会降低10月龄小鼠的突触可塑性并导致记忆障碍。此外，[硒蛋白名称]基因敲除会导致高血糖并扰乱葡萄糖代谢，而葡萄糖代谢对大脑中的突触形成和传递至关重要。进一步的研究表明，[硒蛋白名称]基因敲除会导致大脑胰岛素信号通路[磷脂酰肌醇3激酶（PI3K）/AKT/mTOR/p70 S6激酶通路]受到抑制，这可能会损害小鼠的突触可塑性。高脂饮食（HFD）喂养会抑制[硒蛋白名称]基因敲除小鼠的大脑胰岛素信号通路，并导致5月龄时更早出现认知障碍。总体而言，我们的研究表明，[硒蛋白名称]基因敲除通过大脑胰岛素信号通路诱导突触缺陷，从而导致小鼠认知功能障碍。这些数据强烈表明，[硒蛋白名称]在大脑葡萄糖代谢中起着至关重要的作用，并对突触可塑性有重大贡献。
