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Electrical Pulse Stimulation Partially Restores Insulin Signaling in Palmitate-Induced Insulin-Resistant Skeletal Muscle Cells via Mitochondrial Remodeling and Contractile Activity-Dependent Secretome.

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Title: Electrical Pulse Stimulation Partially Restores Insulin Signaling in Palmitate-Induced Insulin-Resistant Skeletal Muscle Cells via Mitochondrial Remodeling and Contractile Activity-Dependent Secretome.
Authors: Alessandro F; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Sevgican Y; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Mona H; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Patrick S; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Polina L; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Marlene P; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Geronimo H; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Sandra T; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany., Michael R; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany.; Department of Endocrinology and Diabetology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany., Lucia M; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich-Heine-University, Düsseldorf, Germany.; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Neuherberg, Germany.
Source: Journal of cellular physiology [J Cell Physiol] 2026 Oct; Vol. 241 (10), pp. e70240.
Publication Type: Journal Article
Language: English
Journal Info: Publisher: Wiley-Liss Country of Publication: United States NLM ID: 0050222 Publication Model: Print Cited Medium: Internet ISSN: 1097-4652 (Electronic) Linking ISSN: 00219541 NLM ISO Abbreviation: J Cell Physiol Subsets: MEDLINE
Imprint Name(s): Publication: New York, NY : Wiley-Liss
Original Publication: Philadelphia, Wistar Institute of Anatomy and Biology.
MeSH Terms: Insulin*/metabolism , Insulin Resistance*/physiology , Muscle Fibers, Skeletal*/metabolism , Muscle Fibers, Skeletal*/drug effects , Muscle, Skeletal*/metabolism , Muscle, Skeletal*/drug effects , Palmitates*/pharmacology , Muscle Contraction*/drug effects , Muscle Contraction*/physiology , Mitochondria*/metabolism , Mitochondria*/drug effects , Mitochondria, Muscle*/metabolism , Mitochondria, Muscle*/drug effects, Signal Transduction/drug effects ; Electric Stimulation/methods ; Mitochondrial Dynamics/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; GTP Phosphohydrolases/metabolism ; Dynamins/metabolism ; Animals ; Mice ; Cell Line ; Phosphorylation ; Cell Respiration
Abstract: Lipid oversupply induces insulin resistance in skeletal muscle (SkM), partly by altering mitochondrial function and dynamics. Although electrical pulse stimulation (EPS) improves insulin signaling in myotubes, the mechanisms contributing to this effect under lipotoxic conditions remain unclear. Thus, we investigated whether EPS restores lipid-induced insulin resistance in association with changes in mitochondrial respiration and dynamics, lipotoxic intermediates and evaluated the contribution of contraction-induced secreted factors, including small extracellular vesicles (sEV). Murine C2C12 myotubes were treated with palmitate (PA, 0.3 mmol/l) and subjected to EPS (1 Hz, 11.5 V) for 24 h. Insulin signaling, mitochondrial dynamics, respiratory capacity and lipotoxic intermediates were assessed by Western blotting, high-resolution respirometry and liquid chromatography-tandem mass spectrometry in control (CON) and PA-treated cells before and after EPS. Additionally, CON and PA-treated cells were incubated for 24 h with conditioned media and sEV from unstimulated or EPS-stimulated CON and PA-treated cells to evaluate the effect of the myocellular secretome on AKT signaling. PA reduced insulin-stimulated AKT(Ser473) and (Thr308) phosphorylation, which was partially rescued by EPS. In PA cells, EPS decreased the fusion proteins mitofusin 1 and 2 (MFN1, MFN2) and increased the fission marker dynamin-related protein 1 (DRP1). However, mitochondrial respiration and lipid accumulation were unaffected by EPS. Furthermore, conditioned media and sEV from EPS-stimulated cells enhanced AKT phosphorylation in PA-treated cells. These findings demonstrate that attenuation of lipid-induced insulin resistance is independent of mitochondrial respiratory capacity and lipid accumulation, but it is associated with alterations in proteins involved in mitochondrial dynamics and is likely mediated by exercise-derived sEV.
(© 2026 The Author(s). Journal of Cellular Physiology published by Wiley Periodicals LLC.)
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Grant Information: Ministry of Culture and Science of the State of North Rhine-Westfalia (MKW NRW); German Federal Ministry of Health (BMG); Federal Ministry for Research (BMBF)
Contributed Indexing: Keywords: exercise; insulin resistance; mitochondrial dynamics; myokines; skeletal muscle cells
Substance Nomenclature: 0 (Insulin)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
0 (Palmitates)
EC 3.6.1.- (GTP Phosphohydrolases)
EC 3.6.5.5 (Dynamins)
Entry Date(s): Date Created: 20261006 Date Completed: 20261006 Latest Revision: 20261018
Update Code: 20261018
PubMed Central ID: PMC13640965
DOI: 10.1002/jcp.70240
PMID: 42836745
Database: MEDLINE
Description
ISSN:1097-4652
DOI:10.1002/jcp.70240