期刊
AGING-US
卷 11, 期 15, 页码 5726-5743出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.102155
关键词
aging; hyperglycemia; glucose; reactive oxygen species (ROS); SKN-1/Nrf2
资金
- Programs of the National Natural Science Foundation of China [81570808]
- National Key Research and Development Program of China [2017YFC0906903]
- Municipal Human Resources Development Program for Outstanding Leaders in Medical Disciplines in Shanghai [2017BR045]
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.
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