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Key mechanistic features: Selective GHSR-1a agonism Potent GH release without cortisol/ACTH/prolactin elevation Gq/11 Ca signalling Intracellular calcium rise triggers GH exocytosis Pulsatile GH release Preserves physiological GH pulse pattern
Consistency with treatments is key for optimal results, as benefits often improve with time
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d) dagression
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