Watson, J. D. (March 2014) Type 2 diabetes as a redox disease. Lancet, 383 (9919). pp. 841-3. ISSN 0140-6736
Abstract
Physical exercise has long been widely regarded as essential to human health.1 Yet, we do not know how exercise-stressed skeletal muscle cells that generate reactive oxygen species such as hydrogen peroxide (H2O2) delay—if not prevent—the occurrence and severity of diseases such as type 2 diabetes (as well as dementias, cardiovascular disease, and some cancers). Also unexplained is the recent finding that metformin—the most commonly used drug to treat type 2 diabetes2, 3 and 4—and physical exercise seem to be beneficial for several of the same diseases, including cancer, Alzheimer's disease, and cardiovascular disease.5 and 6 New evidence7 shows that combinations of short-term metformin treatment with single acute bouts of exercise do not, as generally expected, enhance insulin sensitivity. In fact, metformin alone can attenuate much of the oxidative effect of exercise.7 The reason why exercise and metformin have opposing physiological consequences (oxidative vs reducing) has been shown by studies 8 that suggest that giving mice metformin increases synthesis of the transcription factor Nrf2, which controls the downstream synthesis of RNA molecules coding for major cellular antioxidant enzymes.
| Item Type: | Paper |
|---|---|
| Subjects: | diseases & disorders > nutritional and metabolic diseases diseases & disorders > nutritional and metabolic diseases > diabetes diseases & disorders > pulmonary disease > oxidative stress |
| CSHL Authors: | |
| Communities: | CSHL labs |
| Depositing User: | Matt Covey |
| Date: | 1 March 2014 |
| Date Deposited: | 07 Mar 2014 16:48 |
| Last Modified: | 07 Mar 2014 16:48 |
| Related URLs: | |
| URI: | https://repository.cshl.edu/id/eprint/29570 |
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