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Systemic inflammation driven by steatosis and necro-inflammatory changes in MASLD activates pathways such as toll-like receptors (TLR) and Nuclear Factor-kappa B (NF-B), causing cardiac and vascular tissue damage
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The cAMP elevation from GHRH-R primes the somatotroph by activating protein kinase A, which phosphorylates voltage-gated calcium channels to increase their open probability, meaning the subsequent calcium surge from GHS-R1a activation encounters a cell already poised for maximal exocytosis
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