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The mechanism partly resembles that found in the pancreatic beta cell, involving closure of ATP-sensitive potassium (K ATP ) channels [14], but in GLUTag cells an additional depolarising stimulus is provided by electrogenic coupled Na + and glucose entry via sodium-coupled glucose cotransporters [15]

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This mechanistic synergy, first characterised in foundational studies of GHRH and GHRP co-administration, provides the physiological and pharmacological rationale for the combination as a research tool for studying maximal physiological GH pulse generation and GH axis pharmacology