Complex regulation of GH autofeedback under dual-peptide drive: studies under a pharmacological GH and sex XXXX clamp.

@entity1 @entity251 @entity7704 @entity53 @entity134 @entity230
To test the postulate that sex difference, sex @entity230 , and peptidyl secretagogues control GH autofeedback, 11 healthy postmenopausal @entity1 and 14 older @entity1 were each given 1) a single iv pulse of GH to enforce negative feedback and 2) continuous iv infusion of saline vs. combined @entity7704 /GHRP-2 to drive feedback escape during pharmacological @entity53 (E(2); @entity1 ) or @entity251 (T; @entity1 ) supplementation vs. placebo in a double-blind, prospectively randomized crossover design. By three-way ANCOVA, sex difference, sex hormone treatment, peptide stimulation, and placebo/saline responses (covariate) controlled total (integrated) GH recovery during feedback (each P < 0.001). Both sex @entity134 milieu (P = 0.019) and dual-peptide stimulation (P < 0.001) determined nadir (maximally feedback-suppressed) GH concentrations. E(2)/T exposure elevated nadir GH concentrations during saline infusion (P = 0.003), whereas dual-peptide infusion did so independently of T/E(2) and sex difference (P = 0.001). All three of sex difference (P = 0.001), sex @entity134 treatment (P = 0.005), and double-peptide stimulation (P < 0.001) augmented recovery of peak (maximally feedback-escaped) GH concentrations. Peak GH responses to dual-peptidyl agonists were greater in @entity1 than in @entity1 (P = 0.016). E(2)/T augmented peak GH recovery during saline infusion (P < 0.001). Approximate entropy analysis corroborated independent effects of sex @entity134 treatment (P = 0.012) and peptide infusion (P < 0.001) on GH regularity. In summary, sex difference, sex @entity134 supplementation, and combined peptide drive influence nadir, peak, and entropic measurements of GH release under controlled negative feedback. To the degree that the pharmacological sex @entity134 , GH, and dual-peptide clamps provide prephysiological regulatory insights, these outcomes suggest major determinants of pulsatile GH secretion in the feedback domain.
