Study summary · research use only
Role of IGF-I in follistatin-induced skeletal muscle hypertrophy
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study (species not stated in the abstract), the authors investigated the role of IGF-I and insulin in follistatin-induced skeletal muscle hypertrophy. The abstract reports that follistatin, a myostatin inhibitor, increased muscle mass while being associated with downregulated muscle IGF-I expression, and retained its full hypertrophic effect in hypophysectomized animals despite very low IGF-I. It states follistatin did not increase muscle sensitivity to IGF-I and that low insulin (via streptozotocin) attenuated the hypertrophic action, which was restored by insulin or IGF-I infusion. The authors conclude follistatin-induced hypertrophy requires activation of the insulin/IGF-I pathway by either insulin or IGF-I, failing only when both are deficient.
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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