ArticleJournal of cachexia, sarcopenia and muscle2025
Zinc Alleviates Diabetic Muscle Atrophy via Modulation of the SIRT1/FoxO1 Autophagy Pathway Through GPR39.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Loss of LCN2 Function Ameliorates Glucocorticoid-Induced Muscle Atrophy via Remodeling the Extracellular Matrix.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Moderate Exercise Mitigates Diabetes-Induced Hippocampal Dysfunction in Aged Rats.International journal of molecular sciences · 2026Article
- A combination of Nrf-2 activator, kinetin and zinc provides neuroprotection through NLRP3-NF-ԟB signaling in traumatic brain injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Brain senescence drives sarcopenia-like transcriptomic remodeling in skeletal muscle.GeroScience · 2026Article
- Parthenolide Attenuates Skeletal Muscle Atrophy Through Regulation of Protein Homeostasis and Inhibition of Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Endoplasmic reticulum stress in skeletal muscle dysfunction of type 2 diabetes: mechanisms and therapeutic implications.Frontiers in endocrinology · 2026Review
- Hysterectomy accelerates sarcopenia risk in US women and mouse models.Frontiers in endocrinology · 2026Article
- Exogenous nanomolar zinc ion (ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- The role of cell death in the physiological and pathological processes of skeletal muscle.Frontiers in physiology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundMuscle atrophy is a severe complication of diabetes, with autophagy playing a critical role in its progression. Zinc has been shown to alleviate hyperglycaemia and several diabetes-related complications, but its direct role in mediating diabetic muscle atrophy remains unclear. This study explores the potential role of zinc in the pathogenesis of diabetic muscle atrophy.
methodsIn vivo, C57BL/6J mice were induced with diabetes by streptozotocin (STZ) and treated with ZnSO₄ (25 mg/kg/day) for six weeks. Gastrocnemius muscles were collected for histological analysis, including transmission electron microscopy (TEM). Serum zinc levels were measured by ICP-MS. Protein expression was evaluated using immunofluorescence (IF), immunohistochemistry (IHC) and Western blotting (WB). Bioinformatics analysis was used to identify key genes associated with muscle atrophy. In vitro, a high-glucose-induced diabetic C2C12 cell model was established and received ZnSO₄, rapamycin, SRT1720, TC-G-1008, or GPR39-CRISPR Cas9 intervention. Autophagy was observed by TEM, and protein expression was assessed by IF and WB. Intracellular zinc concentrations were measured using fluorescence resonance energy transfer (FRET).
resultsIn vivo, muscle atrophy, autophagy activation, and upregulation of SIRT1 and FoxO1, along with downregulation of GPR39, were confirmed in the T1D group. ZnSO₄ protected against muscle atrophy and inhibited autophagy (T1D + ZnSO₄ vs. T1D, all p < 0.0001), as evidenced by increased grip strength (212.40 ± 11.08 vs. 163.90 ± 10.95 gf), gastrocnemius muscle index (10.67 ± 0.44 vs. 8.80 ± 0.72 mg/g), muscle fibre cross-sectional area (978.20 ± 144.00 vs. 580.20 ± 103.30 μm
conclusionZnSO
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