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.