BACKGROUND: Little is known about the pathophysiology of ghrelin secretion in growth hormone-deficient adults treated with growth hormone, and the relationship between plasma ghrelin and hyperinsulinemia induced by an oral glucose load has not been investigated in these patients. OBJECTIVE: In the present study we examined the relationship between plasma ghrelin, insulin, C-peptide and leptin after an oral glucose load in growth hormone-deficient adults receiving treatment with growth hormone. METHODS: Plasma ghrelin, leptin, insulin, C-peptide and blood glucose were measured before and then at 30, 60, 90 and 120 min after the ingestion of glucose (75 g orally) in 20 growth hormone-deficient adults (12 women and 8 men), who had been treated with growth hormone for 7.2 +/- 1.3 years (mean +/- SE). Plasma ghrelin was also determined before and after the glucose load in 10 age-and weight-matched healthy persons (5 women and 5 men). RESULTS: The oral glucose load induced a similar percent suppression of plasma ghrelin in the growth hormone-deficient patients and in the healthy persons. In both groups plasma ghrelin decreased significantly 30 min after the glucose load and remained suppressed throughout the test period. In the patients plasma insulin (baseline, 15.9 +/- 3.9 microIU/ml) and C-peptide (baseline, 2.5 +/- 0.3 ng/ml) showed opposite changes with peak responses at 30 min (insulin, 109.5 +/- 15.6 microIU/ml) or 60 min (C-peptide, 10.3 +/- 1.1 ng/ml). In these patients, post-glucose, but not baseline plasma ghrelin levels correlated negatively with plasma insulin, C-peptide and blood glucose levels, whereas baseline plasma ghrelin correlated inversely with baseline plasma leptin. CONCLUSIONS: The similar suppression of plasma ghrelin in growth hormone-deficient patients treated with growth hormone and in healthy persons after an oral glucose load argues against disturbed regulation of ghrelin secretion in these patients. The correlations between post-glucose plasma ghrelin, insulin and blood glucose support the existence of a previously proposed link between hyperinsulinemia (or increased blood glucose) and suppression of ghrelin levels.
BACKGROUND: Little is known about the pathophysiology of ghrelin secretion in growth hormone-deficient adults treated with growth hormone, and the relationship between plasma ghrelin and hyperinsulinemia induced by an oral glucose load has not been investigated in these patients. OBJECTIVE: In the present study we examined the relationship between plasma ghrelin, insulin, C-peptide and leptin after an oral glucose load in growth hormone-deficient adults receiving treatment with growth hormone. METHODS: Plasma ghrelin, leptin, insulin, C-peptide and blood glucose were measured before and then at 30, 60, 90 and 120 min after the ingestion of glucose (75 g orally) in 20 growth hormone-deficient adults (12 women and 8 men), who had been treated with growth hormone for 7.2 +/- 1.3 years (mean +/- SE). Plasma ghrelin was also determined before and after the glucose load in 10 age-and weight-matched healthy persons (5 women and 5 men). RESULTS: The oral glucose load induced a similar percent suppression of plasma ghrelin in the growth hormone-deficient patients and in the healthy persons. In both groups plasma ghrelin decreased significantly 30 min after the glucose load and remained suppressed throughout the test period. In the patients plasma insulin (baseline, 15.9 +/- 3.9 microIU/ml) and C-peptide (baseline, 2.5 +/- 0.3 ng/ml) showed opposite changes with peak responses at 30 min (insulin, 109.5 +/- 15.6 microIU/ml) or 60 min (C-peptide, 10.3 +/- 1.1 ng/ml). In these patients, post-glucose, but not baseline plasma ghrelin levels correlated negatively with plasma insulin, C-peptide and blood glucose levels, whereas baseline plasma ghrelin correlated inversely with baseline plasma leptin. CONCLUSIONS: The similar suppression of plasma ghrelin in growth hormone-deficient patients treated with growth hormone and in healthy persons after an oral glucose load argues against disturbed regulation of ghrelin secretion in these patients. The correlations between post-glucose plasma ghrelin, insulin and blood glucose support the existence of a previously proposed link between hyperinsulinemia (or increased blood glucose) and suppression of ghrelin levels.
Authors: Polyxeni Koutkia; Bridget Canavan; Michael L Johnson; Alex DePaoli; Steven Grinspoon Journal: Am J Physiol Endocrinol Metab Date: 2003-04-29 Impact factor: 4.310
Authors: J A Janssen; F M van der Toorn; L J Hofland; P van Koetsveld; F Broglio; E Ghigo; S W Lamberts; A Jan van der Lely Journal: Eur J Endocrinol Date: 2001-12 Impact factor: 6.664
Authors: Y Date; M Kojima; H Hosoda; A Sawaguchi; M S Mondal; T Suganuma; S Matsukura; K Kangawa; M Nakazato Journal: Endocrinology Date: 2000-11 Impact factor: 4.736
Authors: Seppo M Pöykkö; Eija Kellokoski; Sohvi Hörkkö; Heikki Kauma; Y Antero Kesäniemi; Olavi Ukkola Journal: Diabetes Date: 2003-10 Impact factor: 9.461
Authors: Vincenzo Cappiello; Cristina Ronchi; Paola S Morpurgo; Paolo Epaminonda; Maura Arosio; Paolo Beck-Peccoz; Anna Spada Journal: Eur J Endocrinol Date: 2002-08 Impact factor: 6.664