Why are you getting A Gh test? A spot GH test is worthless, for the most part. having said that, it would be best to fast.
GH Secretion after Glucose Ingestion in Men
In clinical studies, a rebound-like pattern of GH release begins several hours after oral glucose administration [oral glucose tolerance test (OGTT)]. A similar time delay applies to exogenous glucagon-induced GH release, which also transiently elevates blood glucose concentrations. The mechanisms that control delayed rebound- like GH secretion after glucose ingestion are not known.
GH secretion is supervised by an ensemble of hypothalamic peptides and systemic hormones. Somatostatin is a noncompetitive inhibitor of GH release, whereas GHRH stimulates both GH synthesis and secretion. The GH-releasing peptide (GHRP), ghrelin, amplifies the amount of GH secreted per burst. GHRP’s primary action in vivo is via the regulation of GHRH and somatostatin, although strong GH release is observable in vitro also in primary primate pituitary cell cultures.
Systemic hormones and metabolites may modulate GH secretion directly at the pituitary level and/or indirectly by modifying the release and actions of somatostatin, GHRH, or ghrelin. For example, in the rat, hyperglycemia evokes somatostatin-dependent inhibition of pulsatile GH secretion. In humans, oral glucose administration also suppresses GH concentrations rapidly and markedly inferentially by inhibition of hypothalamic GHRH and/or the stimulation of somatostatin release because GHRP attenuates the inhibitory effect of glucose ingestion.
Suppression of GH release by glucose or somatostatin is followed by rebound-like secretion, resulting in peak GH concentrations above the fasting baseline values. The mechanisms mediating postsomatostatin rebound-like GH peak may include GHRH release and somatostatin withdrawal, which triggers discharge of newly synthesized GH granules.
Iranmanesh A, Lawson D, Veldhuis JD. Distinct Metabolic Surrogates Predict Basal and Rebound GH Secretion after Glucose Ingestion in Men. Journal of Clinical Endocrinology & Metabolism. 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/m2 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 (R2 = 0.088, P = 0.0077). Peak rebound GH concentrations were related positively to adiponectin and negatively to computed tomography-estimated abdominal visceral fat (AVF) (R2 = 0.182, P = 0.00049) after glucose ingestion. Deconvolution analysis showed that SHBG specifically predicted basal (nonpulsatile) GH secretion after glucose exposure (R2 = 0.153, P = 0.00052). In contrast, together exercise history and adiponectin (both positively) and AVF (negatively) predicted pulsatile GH escape after glucose suppression (R2 = 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.
