Distinct metabolic surrogates predict basal and rebound GH secretion after glucose ingestion in men.

Context: GH secretion declines rapidly after glucose ingestion and then recovers to higher-than-baseline levels (rebound GH release).

Hypothesis: Selective metabolic markers predict the magnitude of glucose-suppressed GH release and postglucose rebound-like GH secretion.

Design: Prospectively randomized crossover study of GH secretion after glucose vs. water ingestion.

Setting: The study was conducted at a clinical translational research center.

Participants: Sixty-nine healthy men aged 19-78 yr with a body mass index of 18-39 kg/m(2) participated in the study.

Outcomes: OUTCOMES included nadir vs. peak GH concentrations and basal vs. pulsatile GH secretion.

Results: Mean nadir GH concentrations were determined positively by sex hormone binding globulin (SHBG) after glucose administration (R(2) = 0.088, P = 0.0077). Peak rebound GH concentrations were related positively to adiponectin and negatively to computed tomography-estimated abdominal visceral fat (AVF) (R(2) = 0.182, P = 0.00049) after glucose ingestion. Deconvolution analysis showed that SHBG specifically predicted basal (nonpulsatile) GH secretion after glucose exposure (R(2) = 0.153, P = 0.00052). In contrast, together exercise history and adiponectin (both positively) and AVF (negatively) predicted pulsatile GH escape after glucose suppression (R(2) = 0.206, P = 0.00043). Moreover, adiponectin uniquely determined the size (mass), and AVF the mode (duration), of GH secretory bursts after glucose exposure (both P < 0.006).

Conclusion: Glucose ingestion provides a clinical model for investigating complementary metabolic surrogates that determine suppression and recovery of basal and pulsatile GH secretion in healthy men.