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Title: Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes.

Authors: Carter, Calvin S; Huang, Sunny C; Searby, Charles C; Cassaidy, Benjamin; Miller, Michael J; Grzesik, Wojciech J; Piorczynski, Ted B; Pak, Thomas K; Walsh, Susan A; Acevedo, Michael; Zhang, Qihong; Mapuskar, Kranti A; Milne, Ginger L; Hinton Jr, Antentor O; Guo, Deng-Fu; Weiss, Robert; Bradberry, Kyle; Taylor, Eric B; Rauckhorst, Adam J; Dick, David W; Akurathi, Vamsidhar; Falls-Hubert, Kelly C; Wagner, Brett A; Carter, Walter A; Wang, Kai; Norris, Andrew W; Rahmouni, Kamal; Buettner, Garry R; Hansen, Jason M; Spitz, Douglas R; Abel, E Dale; Sheffield, Val C

Published In Cell Metab, (2020 10 06)

Abstract: 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-to-GSSG 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.

PubMed ID: 33027675 Exiting the NIEHS site

MeSH Terms: Animals; Diabetes Mellitus, Type 2/blood; Diabetes Mellitus, Type 2/metabolism; Diabetes Mellitus, Type 2/therapy*; Electromagnetic Fields/adverse effects*; Female; Homeostasis; Humans; Male; Mice; Mice, Inbred C57BL; Reactive Oxygen Species/metabolism; Tumor Cells, Cultured

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