4.8 Article

Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes

Journal

CELL METABOLISM
Volume 32, Issue 4, Pages 561-+

Publisher

CELL PRESS
DOI: 10.1016/j.cmet.2020.09.012

Keywords

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Funding

  1. Janice and Herbert Wilson Family Foundation
  2. Chris and Charles Chessman Foundation
  3. Roy J. Carver Charitable Trust
  4. American Diabetes Association [119PMF030]
  5. Francois Abboud Cardiovascular Center
  6. University of Iowa Research Foundation
  7. Medical Scientist Training Program NIH [5T32GM007337]
  8. NIH [R01EY11298, R01EY017168, P30EY025580, 1S10OD026835-01, R01 DK104998, R01DK115791, P01 HL084207, R01 HL127764, HL112413]
  9. Holden Comprehensive Cancer Center at The University of Iowa and its National Cancer Institute Award [P30CA086862]
  10. NCI [P01CA217797, P42ES013661, R01CA169046, R01CA182804]
  11. American Diabetes Association postdoctoral fellowship [1-18-PDF-060]
  12. Vanderbilt University Medical Center Diabetes Research and Training Center (NIDDK grant) [DK20593]
  13. Fraternal Order of Eagles Diabetes Research Center
  14. VA Merit grant [BX004249]
  15. Teresa Benoit Diabetes research fund
  16. [F30CA213817]

Ask authors/readers for more resources

Aberrant redox signaling underlies the pathophysiology of many chronic metabolic diseases, including type 2 diabetes (T2D). Methodologies aimed at rebalancing systemic redox homeostasis have had limited success. A noninvasive, sustained approach would enable the long-term control of redox signaling for the treatment of T2D. We report that static magnetic and electric fields (sBE) noninvasively modulate the systemic GSH-toGSSG redox couple to promote a healthier systemic redox environment that is reducing. Strikingly, when applied to mouse models of T2D, sBE rapidly ameliorates insulin resistance and glucose intolerance in as few as 3 days with no observed adverse effects. Scavenging paramagnetic byproducts of oxygen metabolism with SOD2 in hepatic mitochondria fully abolishes these insulin sensitizing effects, demonstrating that mitochondrial superoxide mediates induction of these therapeutic changes. Our findings introduce a remarkable redox-modulating phenomenon that exploits endogenous electromagneto-receptive mechanisms for the noninvasive treatment of T2D, and potentially other redox-related diseases.

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