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

Ali Iranmanesh, Donna Lawson, Johannes D Veldhuis

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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 (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.

Original languageEnglish (US)
Pages (from-to)2172-2179
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume97
Issue number6
DOIs
StatePublished - Jun 2012

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Eating
Glucose
Intra-Abdominal Fat
Adiponectin
Sex Hormone-Binding Globulin
Fats
Translational Medical Research
Deconvolution
Cross-Over Studies
Tomography
Body Mass Index
Exercise
Recovery
Water

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Distinct metabolic surrogates predict basal and rebound GH secretion after glucose ingestion in men. / Iranmanesh, Ali; Lawson, Donna; Veldhuis, Johannes D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 97, No. 6, 06.2012, p. 2172-2179.

Research output: Contribution to journalArticle

Iranmanesh, Ali ; Lawson, Donna ; Veldhuis, Johannes D. / Distinct metabolic surrogates predict basal and rebound GH secretion after glucose ingestion in men. In: Journal of Clinical Endocrinology and Metabolism. 2012 ; Vol. 97, No. 6. pp. 2172-2179.
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abstract = "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 (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.",
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