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Diabetes-associated complications, including retinopathy, neuropathy, and nephropathy are associated with increased glucose levels, but it is not understood how glucose drives these manifestations. There is evidence that cultured cells exposed to high levels of glucose produce reactive oxygen species (ROS); however it is unknown if ROS contributes directly to diabetes complications.
In this issue of the Journal of Clinical Investigation, Kumar Sharma and colleagues at the University of California, San Diego determined that ROS production was actually reduced in kidneys of diabetic mice, and this decrease was associated with lowered activity of the major energy-sensing enzyme, AMPK. Furthermore, AMPK activity was also reduced in kidneys of diabetic patients.
Treatment of diabetic mice with a compound that increased AMPK activity reduced kidney-associated symptoms, including fibrosis and albuminuria.
In the companion commentary, Dwight Towler of the Sanford-Burnham Medical Institute discusses how this view of ROS in diabetes will require a new look at therapeutic approaches for relieving diabetes complications.
ACCOMPANYING COMMENTARY TITLE: Mitochondrial ROS deficiency and diabetic complications: AMP[K]-lifying the adaptation to hyperglycemia
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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