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Aging (Albany NY). 2019 Aug 12;11(15):5726-5743. doi: 10.18632/aging.102155. Epub 2019 Aug 12.

Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival.

Author information

1
Shanghai East Hospital, Tongji University School of Medicine, Department of Endocrinology and Metabolic Disease, Translational Medical Center for Stem Cell Therapy, Shanghai, China.
2
Shanghai Jiao Tong University Affiliated Sixth People's Hospital, The Metabolic Diseases Biobank, Center for Translational Medicine, Shanghai Key Laboratory of Diabetes, Shanghai, China.
3
Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.

Abstract

Carbohydrate overconsumption increases blood glucose levels, which contributes to the development of various diseases including obesity and diabetes. It is generally believed that high glucose metabolism increases cellular reactive oxygen species (ROS) levels, damages insulin-secreting cells and leads to age-associated diabetic phenotypes. Here we find that in contrast, high glucose suppresses ROS production induced by paraquat in both mammalian cells and the round worm C. elegans. The role of glucose in suppressing ROS is further supported by glucose's ability to alleviate paraquat's toxicity on C. elegans development. Consistently, we find that the ROS-regulated transcription factor SKN-1 is inactivated by glucose. As a result, the ROS/SKN-1-dependent lifespan extension observed in paraquat-treated animals, mitochondrial respiration mutant isp-1 and germline-less mutant glp-1 are all suppressed by glucose. Our study reveals an unprecedented interaction of glucose with ROS, which could have significant impact on our current understanding of glucose- and ROS-related diseases.

KEYWORDS:

SKN-1/Nrf2; aging; glucose; hyperglycemia; reactive oxygen species (ROS)

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