# Modulating ROS by Electromagnetic Fields to Treat Type 2 Diabetes

> **NIH NIH R01** · UNIVERSITY OF IOWA · 2024 · $449,766

## Abstract

Abstract
Aberrant redox homeostasis has been proposed to contribute to the pathophysiology of type 2 diabetes
(T2D). However, the mechanisms are poorly understood. Redox systems are regulated by pro-oxidants,
such as reactive oxygen species (ROS) and antioxidants such as glutathione. Patients with T2D have
elevated levels of ROS and lower levels of glutathione. Attempts to reverse this redox imbalance in T2D
using redox-modulating drugs or infusion of antioxidants has shown promise in reversing insulin resistance
in preliminary studies, but ultimately have failed in clinical trials due to their short half-lives and delivery
challenges. New methods and a better understanding of redox mechanisms in T2D are needed to address
an underlying pathophysiology of T2D that is not currently effectively addressed by current modalities. ROS
possess an unpaired electron, making them paramagnetic and capable of interacting with externally applied
electromagnetic fields (EMFs). We recently identified a unique set of EMF parameters that rapidly modulate
ROS and redox homeostasis. When applied to mouse models of T2D and human cells, EMFs were found to
exert remarkable effects on glycemia and insulin sensitivity, reversing glucose intolerance and insulin
resistance in three days, without adverse effects. We also found that application of EMFs altered the
metabolic flux of glucose, increasing glucose incorporation into glycogen and reducing fatty acid levels.
Scavenging paramagnetic ROS or preventing redox adaptations by infusing oxidizing redox solutions
(GSSG) abolished these striking therapeutic effects. These findings lead us to hypothesize that EMFs target
ROS to induce an NRF2-mediated redox response that is insulin sensitizing in part by altering the fate of
glucose. Therefore, the goal of this project is to elucidate the redox and metabolic mechanisms underlying
the insulin sensitizing effects of EMFs. We will test our hypotheses in two specific aims: 1) Determine the
redox mechanisms that mediate the insulin-sensitizing effects of EMF-therapy; and 2) Determine the
mechanisms by which EMF-therapy or redox modulation redirects the metabolic fate of glucose to improve
insulin sensitivity. The use of EMFs as a redox- and glycemia-modulating modality provides an
unprecedented opportunity to study the role of redox in T2D pathophysiology and to advance the
understanding of a novel, insulin sensitizing phenomenon. We will identify specific metabolic changes that
occur in response to EMF exposure and determine mechanisms by which the redox state regulates hepatic
metabolic flux and insulin sensitivity. This work will identify a novel mechanistic link between two previously
disconnected fields of inquiry, static EMFs and glycemic regulation and will bridge redox biology with
glucose metabolism. Successful completion of this work will lay the foundation for the future clinical
development of a wearable device that emits EMFs to target redox systems for the noninvasiv...

## Key facts

- **NIH application ID:** 10775773
- **Project number:** 5R01DK125079-04
- **Recipient organization:** UNIVERSITY OF IOWA
- **Principal Investigator:** E Dale Abel
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $449,766
- **Award type:** 5
- **Project period:** 2021-04-15 → 2026-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10775773

## Citation

> US National Institutes of Health, RePORTER application 10775773, Modulating ROS by Electromagnetic Fields to Treat Type 2 Diabetes (5R01DK125079-04). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10775773. Licensed CC0.

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