Potential Protective Effect of Dietary Intake of Non-α-Tocopherols on Cellular Aging Markers Mediated by Tumor Necrosis Factor-α in Prediabetes: A Cross-Sectional Study of Chinese Adults. (15th May 2020)

• Record Type: Journal Article
• Authors: Liu, Yiwen; Ma, Chifa; Li, Pingping; Ma, Chunxiao; He, Shuli; Ping, Fan; Zhang, Huabing; Li, Wei; Xu, Lingling; Li, Yuxiu
• Other Names: Morales Patricia Guest Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2020(2020)
• Publication Date: 2020-05-15
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2020/7396801
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : It remains unknown how different glucose tolerance status affects the relationships between dietary intake of different tocopherol isoforms ( α -, β -, γ -, and δ -tocopherol) and cellular aging, oxidative stress, and inflammatory markers. The authors conducted a cross-sectional study among 582 Chinese adults with different glucose tolerance status to explore the association between dietary intake of different tocopherol isoforms and cellular aging, oxidative stress, and inflammatory markers. The inverse correlations between non- α -tocopherols and tumor necrosis factor-alpha (TNF- α ) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r = − 0.33 for β -/ γ -tocopherol, r = − 0.37 for δ -tocopherol, p < 0.01 ), followed by normal glucose tolerance (NGT). While such correlations were abolished in established diabetes. Furthermore, within prediabetes, the strongest inverse correlations between non- α -tocopherols and TNF- α were observed in impaired fasting glucose (IFG) (r = − 0.42 for β -/ γ -tocopherol, r = − 0.55 for δ -tocopherol, p < 0.01 ), while such correlations were significantly attenuated in individuals with impaired glucose tolerance (IGT) and IFG+IGT. And mediation model analysis displayed that TNF- α mediated the protective effect of non- α -tocopherols on leukocyte telomere length and mitochondrial DNA copy number, which was uniquely observed in prediabetes, while such mediation effect was statistically nonsignificant in NGT and established diabetes. In conclusion, our findings indicate that dietary intake of non- α -tocopherols might protect against cellular aging markers mediated by TNF- α in prediabetes. Individuals with prediabetes, especially for IFG, might benefit from increasing dietary intake of non- α -tocopherol in alleviating inflammation and cellular aging, which might provide a new dietary avenue for delaying diabetes onset.