Source comparison
IGF-1 Dynamics: Pulse vs Plateau Biology
IGF-1 is produced primarily in the liver in response to GH-activated GHR-JAK2-STAT5b signalling. The temporal dynamics of GH delivery determine the IGF-1 production kinetics and consequently IGFBP-1 suppression, free IGF-1 availability and tissue IGF-1R engage
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- IGF-1 is produced primarily in the liver in response to GH-activated GHR-JAK2-STAT5b signalling. The temporal dynamics of GH delivery determine the IGF-1 production kinetics and consequently IGFBP-1 suppression, free IGF-1 availability and tissue IGF-1R engagement duration.
- Sermorelin IGF-1 dynamics: Daily Sermorelin produces circulating IGF-1 elevation of +28-38% from baseline in aged somatopause models after 4 weeks of daily dosing. The hepatic STAT5b activation pattern is pulsatile: peak STAT5b-pTyr694 at 2-3h post-injection, returning to baseline at 6-8h. IGFBP-1 (hepatic production, GH-suppressed) shows 4-6h suppression nadir post-injection followed by rebound — maintaining the IGFBP-1 diurnal oscillation that regulates free IGF-1 availability. This oscillation is biologically relevant to tissue IGF-1R internalisation kinetics: pulsatile free IGF-1 availability (peaks and troughs) maintains IGF-1R surface expression through receptor recycling between peaks.
- CJC-1295 DAC IGF-1 dynamics: Single injection produces sustained IGF-1 elevation +40-50% for 14 days. STAT5b activation is tonic (continuous low-level pTyr694, +28-34% above baseline throughout 7 days). IGFBP-1 suppression: sustained (−28-34% throughout 14 days, no diurnal oscillation). The consequence: continuous free IGF-1 elevation → sustained IGF-1R occupancy → receptor downregulation (surface IGF-1R −18-24% by day 7 in peripheral tissues) — the same receptor desensitisation paradox observed with continuous rhGH infusion versus pulsatile GH delivery. The desensitisation is partial and reversible but represents a meaningful mechanistic disadvantage for sustained anabolic signalling.