Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes

Carter, Calvin S.; Huang, Haigen; Searby, Charles; Cassaidy, Benjamin; Miller, Michael J.; Grzesik, Wojciech J.; Piorczynski, Ted B.; Pak, Thomas; Walsh, Susan A.; Acevedo, Michael; Zhang, Qihong; Mapuskar, Kranti A.; Milne, Ginger L.; Hinton, Antentor; Guo, Deng‐Fu; Weiss, Robert G.; Bradberry, Kyle; Taylor, Eric B.; Rauckhorst, Adam J.; Dick, David; 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.

doi:10.1016/j.cmet.2020.09.012

Cited by 61 publications

(47 citation statements)

References 87 publications

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“…Both studies implicate that magnetic fields might directly interfere with hypoxic signaling in vivo. In addition, the ability of EMF to treat type 2 diabetes in mice (Carter et al 2020) strongly underpins our findings, given that the cellular glucose metabolism is mainly controlled by HIF-1α.…”

Section: Discussionsupporting

confidence: 70%

“…Several groups have been investigating the impact of low intensity electromagnetic fields (EMFs) on biological systems, as potential therapeutic tools (Carter et al 2020;Cook et al 2015;Kiss et al 2015;Markov 2015;Morris and Skalak 2008;Rose et al 2016;Vadala et al 2016) or as possible environmental hazards (Juutilainen et al 2018;Kaszuba-Zwoinska et al 2015;Vanderstraeten et al 2012Vanderstraeten et al , 2015World Health Organization 2007). Special interest was thereby given to the influence of low-intensity EMFs on circadian clocks, and here, in particular, on the flavoprotein family of Cryptochromes (Crys).…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic Nuclear Magnetic Resonance affects the core clock mechanism and associated Hypoxia-inducible factor-1

Thöni

Oliva

Mauracher

et al. 2021

Chronobiology International

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The influence of low intensity electromagnetic fields on circadian clocks of cells and tissues has gained increasing scientific interest, either as a therapeutic tool or as a potential environmental hazard. Nuclear Magnetic Resonance (NMR) refers to the property of certain atomic nuclei to absorb the energy of radio waves under a corresponding magnetic field. NMR forms the basis for Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy and, in a low-intensity form, for NMR therapy (tNMR). Since the circadian clock is bi-directionally intertwined with hypoxic signaling in vertebrates and mammals, we hypothesized that low intensity electromagnetic fields, such as tNMR, might not only affect circadian clocks but also Hypoxia-Inducible Factor-1α (HIF-1α). As master regulator of the hypoxic signaling pathway, HIF-1α is known to dampen the circadian amplitude under reduced oxygen availability, while the hypoxic response of cells and organisms, itself, is tightly clock controlled. In a first experiment, we investigated if tNMR is able to act as Zeitgeber for the core clock mechanism of unsynchronized zebrafish and mouse fibroblast cells, using direct light irradiation and treatment with the glucocorticoid Dexamethasone as references. tNMR significantly affected the cell autonomous clocks of unsynchronized mouse fibroblast cells NIH3-T3, but did not act as a Zeitgeber. Similar to light irradiation and in contrast to treatment with Dexamethasone, tNMR did not synchronize expression profiles of murine clock genes. However, irradiation with tNMR as well as light significantly altered mRNA and protein expression levels of Cryptochrome1, Cryptochrome2 and Clock1 for more than 24 h. Changes in mRNA and protein after different treatment durations, namely 6 and 12 h, appeared to be nonlinear. A nonlinear doseresponse relationship is known as hallmark of electromagnetic field induced effects on biological systems. The most prominent alterations were detected in murine HIF-1α protein, again in a nonlinear dose-response. In contrast to murine cells, zebrafish fibroblasts did not respond to tNMR at all. Light, a potent Zeitgeber for the peripheral clocks of fish, led to the expected synchronized clock gene oscillations of high amplitude, as did Dexamethasone. Hence, we conclude, mammalian peripheral clocks are more susceptible to tNMR than the direct light entrainable fish fibroblasts. Although light and tNMR did not act as Zeitgebers for the circadian clocks of unsynchronized murine cells, the significant observed effects might indicate downstream cellphysiological ramifications, which are worth future investigation. However, beside the effects tNMR exerts on the core clock mechanism of mammalian cells, the technology might be the first non-pharmacological approach to modify HIF-1α protein in cells and tissues. HIF-1α and the associated circadian clock play key roles in diseases with underlying ischemic background, such as infarct, stroke, and cancer and, also infectious diseases, such as Covid-19. Hence, low intensity magnet...

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Therapeutic Nuclear Magnetic Resonance affects the core clock mechanism and associated Hypoxia-inducible factor-1

Thöni

Oliva

Mauracher

et al. 2021

Chronobiology International

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“…In other words, its overall downregulation will affect the ATP production and other important metabolic pathways (Gaster et al, 2012). The pivotal role of mitochondrial RET in T2D was highlighted in a recent study that successfully treated T2D in mice models using magnetic and electric fields (Carter et al, 2020). The impairment of the TCA cycle and the RET chain in VAT and skeletal muscle of T2D subjects compared to CTRL and PD, in combination with the indistinguishable differences between CTRL and PD suggested a relatively late event becoming evident when diabetes is already established, rather than during its development (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes and normal tissues

Diamanti

Cavalli

Pereira

et al. 2021

Preprint

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Defects in pancreatic islets and the progression of multi-tissue insulin resistance in combination with environmental factors are the main causes of type 2 diabetes (T2D). Mass spectrometry-based proteomics of five key-metabolic tissues on a cohort of 42 multi-organ donors provided deep coverage of the proteomes of pancreatic islets, visceral adipose tissue (VAT), liver, skeletal muscle and serum. Enrichment analysis of gene ontology (GO) terms built a tissue-specific map of the chronological order of altered biological processes across healthy controls (CTRL), pre-diabetes (PD) and T2D subjects. This unique dataset allowed us to explore alterations of entire biological pathways and individual proteins in multiple tissues. We confirmed the significant decrease of the citric acid cycle and the respiratory electron transport in VAT and muscle of T2D and we provided a thorough visual representation of the complete set of downregulated proteins. Importantly, we found widespread novel alterations in relevant biological pathways including the increase in hemostasis in pancreatic islets of PD, the increase in the complement cascade in liver and pancreatic islets of PD and the elevation in cholesterol biosynthesis in liver of T2D. Overall, our findings suggest inflammatory, immune and vascular impairments in pancreatic islets as potentially causal factors of insufficient insulin production and increased glucagon levels in the early stages of T2D. In contrast alterations in lipid metabolism and mitochondrial function in the liver and VAT/muscle, respectively, became evident later in manifest T2D. This first multi-tissue proteomic map indicates the temporal order of tissue-specific metabolic dysregulation in T2D development.

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“…Therefore, coordinates of pixels are annotated p1 = (x1, y1) and p2 = (x2, y2) for pixels 1 and 2. Measurements needed to decipher the changes in organelle morphology were constructed using the following calculations [12][13][14][15][16][17][18][19][20][21]:…”

Section: Imagej Quantificationmentioning

confidence: 99%

A Universal Approach to Analyzing Transmission Electron Microscopy with ImageJ

Lam

Katti

Biete

et al. 2021

Cells

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112

146

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Transmission electron microscopy (TEM) is widely used as an imaging modality to provide high-resolution details of subcellular components within cells and tissues. Mitochondria and endoplasmic reticulum (ER) are organelles of particular interest to those investigating metabolic disorders. A straightforward method for quantifying and characterizing particular aspects of these organelles would be a useful tool. In this protocol, we outline how to accurately assess the morphology of these important subcellular structures using open source software ImageJ, originally developed by the National Institutes of Health (NIH). Specifically, we detail how to obtain mitochondrial length, width, area, and circularity, in addition to assessing cristae morphology and measuring mito/endoplasmic reticulum (ER) interactions. These procedures provide useful tools for quantifying and characterizing key features of sub-cellular morphology, leading to accurate and reproducible measurements and visualizations of mitochondria and ER.

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Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes

Cited by 61 publications

References 87 publications

Therapeutic Nuclear Magnetic Resonance affects the core clock mechanism and associated Hypoxia-inducible factor-1

Therapeutic Nuclear Magnetic Resonance affects the core clock mechanism and associated Hypoxia-inducible factor-1

Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes and normal tissues

A Universal Approach to Analyzing Transmission Electron Microscopy with ImageJ

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