IGF-1 Cascade Support involves interventions aimed at optimizing the signaling pathway initiated by Insulin-like Growth Factor 1 (IGF-1), which is largely mediated by the liver in response to Growth Hormone (GH). This support is crucial for tissue anabolism, cellular proliferation, and skeletal maintenance, particularly in aging populations. Clinical efforts focus on ensuring adequate upstream GH secretion and downstream receptor sensitivity to IGF-1. Insufficient cascade activity is associated with sarcopenia and impaired repair processes.
Origin
The term stems directly from the somatotropic axis where Growth Hormone stimulates hepatic IGF-1 production, initiating the cascade. “Support” implies providing the necessary physiological conditions—nutritional status, insulin sensitivity, and GH availability—for this pathway to function optimally. The cascade itself describes the sequence of molecular events downstream of IGF-1 binding.
Mechanism
The core mechanism involves GH binding to its receptor, triggering the release of IGF-1, which then acts in an endocrine or autocrine/paracrine manner by binding to the IGF-1 receptor. This binding activates intracellular signaling, notably the Akt/mTOR pathway, promoting protein synthesis and inhibiting apoptosis. Supporting this cascade requires optimizing nutritional intake, particularly adequate protein and essential cofactors, to ensure substrate availability for GH action.
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