ArticleJournal of cachexia, sarcopenia and muscle2021
Modified UCN2 peptide treatment improves skeletal muscle mass and function in mouse models of obesity-induced insulin resistance.
Article in Journal of cachexia, sarcopenia and muscle, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Comparative Whole Genome Analysis and Targeted Validation of Variants in Three Greek Indigenous Sheep Breeds.Current issues in molecular biology · 2026Article
- GLP-1 Receptor Agonist-Associated Weight Loss and Aesthetic Breast Surgery: A Narrative Review and Experience-Based Recommendations for Plastic and Reconstructive Surgeons.Aesthetic surgery journal. Open forum · 2026Article
- The metabolic role of corticotropin-releasing hormone receptor 2 and its UCN peptides: emerging therapeutic potential.Skeletal muscle · 2025Review
- Mechanomedicine for Addressing Skeletal Muscle Insulin Resistance.Endocrine reviews · 2025Review
- Maternal Supplementation of Collagen Peptide Chelated Trace Elements Enhances Skeletal Muscle Development in Chicks.Biological trace element research · 2025Article
- Chronic UCN2 treatment desensitizes CRHR2 and improves insulin sensitivity.Nature communications · 2023Article
- Musclin prevents depression-like behavior in male mice by activating urocortin 2 signaling in the hypothalamus.Frontiers in endocrinology · 2023Article
- Urocortin 2 promotes hypertrophy and enhances skeletal muscle function through cAMP and insulin/IGF-1 signaling pathways.Molecular metabolism · 2022Article
- Beyond appetite regulation: Targeting energy expenditure, fat oxidation, and lean mass preservation for sustainable weight loss.Obesity (Silver Spring, Md.) · 2022Review
- Oxidative stress and metabolic diseases: Relevance and therapeutic strategies.Frontiers in nutrition · 2022Review
- Modified UCN2 peptide treatment improves skeletal muscle mass and function in mouse models of obesity-induced insulin resistance.Journal of cachexia, sarcopenia and muscle · 2021Article
- The Critical Role of Oxidative Stress in Sarcopenic Obesity.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundType 2 diabetes and obesity are often seen concurrently with skeletal muscle wasting, leading to further derangements in function and metabolism. Muscle wasting remains an unmet need for metabolic disease, and new approaches are warranted. The neuropeptide urocortin 2 (UCN2) and its receptor corticotropin releasing factor receptor 2 (CRHR2) are highly expressed in skeletal muscle and play a role in regulating energy balance, glucose metabolism, and muscle mass. The aim of this study was to investigate the effects of modified UCN2 peptides as a pharmaceutical therapy to counteract the loss of skeletal muscle mass associated with obesity and casting immobilization.
methodsHigh-fat-fed mice (C57Bl/6J; 26 weeks old) and ob/ob mice (11 weeks old) were injected daily with a PEGylated (Compound A) and non-PEGylated (Compound B) modified human UCN2 at 0.3 mg/kg subcutaneously for 14 days. A separate group of chow-fed C57Bl/6J mice (12 weeks old) was subjected to hindlimb cast immobilization and, after 1 week, received daily injections with Compound A. In vivo functional tests were performed to measure protein synthesis rates and skeletal muscle function. Ex vivo functional and molecular tests were performed to measure contractile force and signal transduction of catabolic and anabolic pathways in skeletal muscle.
resultsSkeletal muscles (extensor digitorum longus, soleus, and tibialis anterior) from high-fat-fed mice treated with Compound A were ~14% heavier than muscles from vehicle-treated mice. Chronic treatment with modified UCN2 peptides altered the expression of structural genes and transcription factors in skeletal muscle in high-fat diet-induced obesity including down-regulation of Trim63 and up-regulation of Nr4a2 and Igf1 (P < 0.05 vs. vehicle). Signal transduction via both catabolic and anabolic pathways was increased in tibialis anterior muscle, with increased phosphorylation of ribosomal protein S6 at Ser
conclusionsModified human UCN2 is a pharmacological candidate for the prevention of the loss of skeletal muscle mass associated with obesity and immobilization.
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