ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Role of IGF-I in follistatin-induced skeletal muscle hypertrophy.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Systematic Review of Sarcopenia Biomarkers in Hip Fracture Patients as a Potential Tool in Clinical Evaluation.International journal of molecular sciences · 2024Pooled it
- Discovery of intestinal microorganisms that affect the improvement of muscle strength.Scientific reports · 2025Article
- Comprehensive Review of Sepsis-Related Skeletal Muscle Atrophy: Mechanisms, Diagnosis and Therapeutic Strategies.Journal of inflammation research · 2025Review
- Whole methylomes reveal high-altitude-associated methylation at hypoxia and pigmentation genes in South American Indigenous populations.Environmental epigenetics · 2025Article
- Blood flow restriction training: a new approach for preventing and treating sarcopenia in older adults.Frontiers in physiology · 2025Review
- Exercise as a Therapeutic Strategy for Obesity: Central and Peripheral Mechanisms.Metabolites · 2024Review
- Extra Virgin Olive Oil (EVOO), a Mediterranean Diet Component, in the Management of Muscle Mass and Function Preservation.Nutrients · 2022Review
- Article
- p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition.Frontiers in physiology · 2021Article
- Review
- Effects of aerobic and inspiratory training on skeletal muscle microRNA-1 and downstream-associated pathways in patients with heart failure.Journal of cachexia, sarcopenia and muscle · 2020Article
- Exercise and Muscle Atrophy.Advances in experimental medicine and biology · 2020Review
- Roles of myokines in exercise-induced improvement of neuropsychiatric function.Pflugers Archiv : European journal of physiology · 2019Review
- Hepatokines-a novel group of exercise factors.Pflugers Archiv : European journal of physiology · 2019Review
- Skeletal Muscle Hypertrophy, Insulin-like Growth Factor 1, Myostatin and Follistatin in Healthy and Sarcopenic Elderly Men: The Effect of Whole-body Resistance Training.International journal of preventive medicine · 2019Article
- α-Ketoglutarate prevents skeletal muscle protein degradation and muscle atrophy through PHD3/ADRB2 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Reduced skeletal muscle fiber size following caloric restriction is associated with calpain-mediated proteolysis and attenuation of IGF-1 signaling.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Downregulated Translation Initiation Signaling Predisposes Low-Birth-Weight Neonatal Pigs to Slower Rates of Muscle Protein Synthesis.Frontiers in physiology · 2017Article
- Glucocorticoids Enhance Muscle Proteolysis through a Myostatin-Dependent Pathway at the Early Stage.PloS one · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Follistatin, a physiological inhibitor of myostatin, induces a dramatic increase in skeletal muscle mass, requiring the type 1 IGF-I receptor/Akt/mTOR pathway. The aim of the present study was to investigate the role of IGF-I and insulin, two ligands of the IGF-I receptor, in the follistatin hypertrophic action on skeletal muscle. In a first step, we showed that follistatin increases muscle mass while being associated with a downregulation of muscle IGF-I expression. In addition, follistatin retained its full hypertrophic effect toward muscle in hypophysectomized animals despite very low concentrations of circulating and muscle IGF-I. Furthermore, follistatin did not increase muscle sensitivity to IGF-I in stimulating phosphorylation of Akt but, surprisingly, decreased it once hypertrophy was present. Taken together, these observations indicate that increased muscle IGF-I production or sensitivity does not contribute to the muscle hypertrophy caused by follistatin. Unlike low IGF-I, low insulin, as obtained by streptozotocin injection, attenuated the hypertrophic action of follistatin on skeletal muscle. Moreover, the full anabolic response to follistatin was restored in this condition by insulin but also by IGF-I infusion. Therefore, follistatin-induced muscle hypertrophy requires the activation of the insulin/IGF-I pathway by either insulin or IGF-I. When insulin or IGF-I alone is missing, follistatin retains its full anabolic effect, but when both are deficient, as in streptozotocin-treated animals, follistatin fails to stimulate muscle growth.
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