Fucoidan prevents diabetic cognitive dysfunction via promoting TET2-mediated active DNA demethylation in high-fat diet induced diabetic mice.

Autor: Chen L; School of Health and life Sciences, University of Health and Rehabilitation Sciences, China., Li Y; School of Public health, Qingdao University, Qingdao, China., Zhang X; School of Public health, Qingdao University, Qingdao, China., Du X; People's Hospital of Gaomi, Weifang, China., Zhang Y; School of Public health, Qingdao University, Qingdao, China., Li X; School of Public health, Qingdao University, Qingdao, China., Zhong Z; Hedong District Center for Disease Control and Prevention, Tianjin, China., Zhou C; State Key Laboratory of Bio-Fibers and Eco-Textiles, Qingdao University, China., Liu X; State Key Laboratory of Bio-Fibers and Eco-Textiles, Qingdao University, China., Wang J; School of Food and Drug, Shenzhen Polytechnic University, Shenzhen, China. Electronic address: junwangwh@hotmail.com., Wang Q; School of Public health, Qingdao University, Qingdao, China. Electronic address: kevin_1971@126.com.
Jazyk: angličtina
Zdroj: International journal of biological macromolecules [Int J Biol Macromol] 2024 Oct; Vol. 278 (Pt 3), pp. 134186. Date of Electronic Publication: 2024 Aug 20.
DOI: 10.1016/j.ijbiomac.2024.134186
Abstrakt: Diabetic cognitive dysfunction (DCD) refers to cognitive impairment in individuals with diabetes, which is one of the most important comorbidities and complications. Preliminary evidence suggests that consuming sufficient dietary fiber could have benefits for both diabetes and cognitive function. However, the effect and underlying mechanism of dietary fiber on DCD remain unclear. We conducted a cross-sectional analysis using data from NHANES involving 2072 diabetics and indicated a significant positive dose-response relationship between the dietary fiber intake and cognitive performance in diabetics. Furthermore, we observed disrupted cognitive function and neuronal morphology in high-fat diet induced DCD mice, both of which were effectively restored by fucoidan supplementation through alleviating DNA epigenetic metabolic disorders. Moreover, fucoidan supplementation enhanced the levels of short-chain fatty acids (SCFAs) in the cecum of diabetic mice. These SCFAs enhanced TET2 protein stability by activating phosphorylated AMPK and improved TETs activity by reducing the ratio of (succinic acid + fumaric acid)/ α-ketoglutaric acid, subsequently enhancing TET2 function. The positive correlation between dietary fiber intake and cognitive function in diabetics was supported by human and animal studies alike. Importantly, fucoidan can prevent the occurrence of DCD by promoting TET2-mediated active DNA demethylation in the cerebral cortex of diabetic mice.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE