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

Abstract

GH secretion declines rapidly after glucose ingestion and then recovers to higher-than-baseline levels (rebound GH release). Selective metabolic markers predict the magnitude of glucose-suppressed GH release and postglucose rebound-like GH secretion. Prospectively randomized crossover study of GH secretion after glucose vs. water ingestion. The study was conducted at a clinical translational research center. Sixty-nine healthy men aged 19-78 yr with a body mass index of 18-39 kg/m(2) participated in the study. OUTCOMES included nadir vs. peak GH concentrations and basal vs. pulsatile GH secretion. 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). 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.