I understand both get grouped as 'GH secretagogues' but I clearly don't understand them well because I keep reading they work through different receptors. Can someone break down the actual mechanism difference without me needing a biochem degree?
Specifically I'm confused about why they're described as complementary. If they both raise GH, why would the pathway matter? Purely trying to understand the biology here, not asking about combining anything.
Good question and the receptor distinction is the whole point. Your pituitary releases GH in pulses, gated by two upstream signals. GHRH (the natural hormone CJC-1295 mimics) is the 'go' signal that tells somatotroph cells to release GH. Separately, the ghrelin receptor (GHS-R) is a different lever — ghrelin and the synthetic GHRPs/ipamorelin act there, and they also suppress somatostatin, which is the body's 'stop' brake on GH.
So one class pushes the accelerator (GHRH pathway) and the other both pushes a second accelerator and eases off the brake (ghrelin pathway). That's why they're described as acting through distinct receptors. I'd stop short of saying more than that here since we don't do combining discussion, but mechanistically that's the picture. Ipamorelin gets singled out because it's relatively selective and doesn't spill over into cortisol/prolactin the way some older GHRPs can.
All of this is still 'raises GH secretion' — translating that to real-world muscle in healthy adults is a much weaker evidence chain.
The accelerator-vs-brake framing finally made it click. Appreciate you drawing the line at mechanism and not going further — that's genuinely all I was after.
Bookmarking this. Every other explanation I found either hand-waved 'they synergize' or dumped a wall of pituitary physiology. This was the middle ground.
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