Oral Glucose Inhibits Growth Hormone Secretion Induced by Human Pancreatic Growth Hormone Releasing Factor 1–44 in Normal Man

Davies, R.R.; Turner, Steve; Johnston, Desmond G.

doi:10.1111/j.1365-2265.1984.tb03235.x

Cited by 49 publications

(28 citation statements)

References 14 publications

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“…In the human, acute hyperglycemia blocks GHRH-induced GH release, which excludes the possibility that glucose may act by inhibiting endogenous GHRH release (3,4,28). These reports suggested that glucose might act in a manner similar to free fatty acids (29), that is, by directly inhibiting pituitary somatotropes or by inducing hypothalamic SRIH release, or by a combination of both mechanisms.…”

Section: Discussionmentioning

confidence: 92%

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Park

Yang²,

Woo³

et al. 2003

European Journal of Endocrinology

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Objective: Acute hyperglycemia stimulates somatostatin (SRIH) release by the hypothalamus which, in turn, suppresses growth hormone (GH) secretion from the anterior pituitary gland. Although it has been suggested that the cholinergic pathway mediates glucose-induced SRIH release, other regulatory systems have not been examined. Therefore, we investigated whether blocking or activating the b-adrenergic pathway alters glucose-mediated inhibition of GH release. Design and methods: One set of experiments was performed with a b-adrenergic antagonist, propranolol, and the other set with a b-adrenergic agonist, isoproterenol. Each set of experiments was performed in ten healthy subjects and consisted of four tests. Test 1, a 100 mg GHRH bolus i.v. at 0 min; test 2, 100 g glucose orally at 2 30 min, followed by a 100 mg GHRH bolus at 0 min; test 3, after a 100 mg GHRH bolus i.v. at 0 min, a continuous infusion of propranolol (0.2 mg/kg) or isoproterenol (0.012 mg/kg) was administered between 0 and 120 min; test 4, after a 100 g glucose oral load at 230 min, and a 100 mg GHRH bolus i.v. at 0 min, a continuous infusion of propranolol (0.2 mg/kg) or isoproterenol (0.012 mg/kg) was administered between 0 and 120 min. Blood was drawn every 10 min from 2 30 min to 120 min to measure GH and glucose concentrations. Results: Pretreatment with glucose significantly suppressed GHRH-induced GH secretion. Propranolol infusion significantly increased the GHRH-induced GH secretion, but it did not block glucose-induced suppression of GH secretion. Isoproterenol infusion alone significantly suppressed GHRH-induced GH secretion and augmented the inhibitory action of glucose on GH release. Conclusion: This study demonstrates that glucose-induced suppression of GHRH-stimulated GH release is independent of b-adrenergic tone. Since previous data supports a role for SRIH in both glucose and b-adrenergic suppression of GH release, the current results suggest that subsets of SRIH neurons are differentially responsive to these external cues. Therefore, a combined glucose and isoproterenol test may provide a useful assessment of hypothalamic somatostatinergic activity.

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Section: Discussionmentioning

confidence: 92%

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Park

Yang²,

Woo³

et al. 2003

European Journal of Endocrinology

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“…However, the mechanism of the suppressing effect of hyperglycemia on GH secretion in normal subjects is not clear, nor is the cause of paradoxical secretion to oral glucose in acromegaly [13][14][15]. It was reported that an acromegaly induced by an ectopic GRHproducing tumor, had a paradoxical GH secretion to oral glucose, but that an exogenous GRH load did not induce GH secretion, therefore GRH was thought not to be involved in the paradoxical GH response to oral glucose load in acromegaly [16].…”

Section: Discussionmentioning

confidence: 99%

Glucose-Dependent Insulinotropic Polypeptide Induced Growth Hormone Secretion in Acromegaly

Umahara¹,

Okada

Ohshima

et al. 2003

Endocr J

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Abstract. Glucose-dependent insulinotropic polypeptide (GIP), a peptide released from the intestines after meals, is thought to stimulate insulin secretion. GIP receptor cDNA has recently been cloned and its mRNA has been recognized in several organs including the pituitary, but the physiological roles of GIP receptors of the pituitary have yet to be determined. We have demonstrated the possibility that GIP stimulates GH secretions from the pituitary adenoma cells of acromegalics. GIP-stimulated GH responses were studied in four acromegalics. In two acromegalics whose GH showed paradoxical secretion to oral glucose tolerance test (OGTT), GIP infusion (0.6 mg/kg/h) drove GH secretion (13.7 to 68.1, 22.5 to 76.2 ng/ml, respectively). However, in the other two acromegalics whose GH showed no paradoxical response to OGTT, GIP infusion did not induce GH secretion. One of the patients who was studied extensively had a GH that responded to OGTT. This patient's serum GH levels increased after meals while adenomectomy abolished both the paradoxical GH secretions by OGTT and GH responses to the GIP infusion. These data suggested that some somatotroph adenoma cells have an aberrant response to GIP which may go toward explaining paradoxical GH secretions to OGTT in acromegalics.

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“…For this reason, before the development of accurate assays for IGF-I measurement, dynamic testing of the GH response to glucose suppression had been used extensively to provide evidence of normal GH secretory dynamics (18,19). Acute elevation of plasma glucose is known to suppress plasma GH secretion in normal subjects (15,20,21). This suppression may be mediated through glucoreceptors in the ventromedial nucleus of the hypothalamus partly via a rise in hypothalamic somatostatin secretion (22)(23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Disease Status with Sensitive Measures of Growth Hormone Secretion in 60 Postoperative Patients with Acromegaly¹

Freda

Post

Powell

et al. 1998

The Journal of Clinical Endocrinology & Metabolism

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Traditionally, suppression of GH measured by polyclonal RIA to less than 2.0 g/L after oral glucose was accepted as evidence of remission after transsphenoidal surgery for acromegaly. Recently, with newer, more sensitive GH assays, a cut-off of less than 1.0 g/L has been suggested. With the development of accurate insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) assays, additional tools are now available for assessing postoperative GH secretion. There has, however, never been a systematic comparison of sensitive GH, IGF-I, and IGFBP-3 assays in defining disease status in a large cohort of postoperative patients with acromegaly. Therefore, we evaluated how the use of modern assays impacts on our assessment of disease activity in these patients.Sixty postoperative subjects with acromegaly and 25 age-matched healthy subjects were evaluated with nadir GH levels after 100 g oral glucose as well as baseline IGF-I and IGFBP-3 levels. GH was assayed by polyclonal RIA, sensitive immunoradiometric assay (IRMA), and highly sensitive enzyme-linked immunosorbent assay. The mean nadir GH determined by IRMA was 0.09 Ϯ 0.004 g/L in the healthy subjects, with the upper limit of the normal nadir being 0.14 g/L (mean ϩ 2 SD). Subjects with acromegaly were divided into those with active disease (n ϭ 22), defined by elevated IGF-I levels, and those in remission (n ϭ 38), defined by normal IGF-I levels. GH determined by IRMA failed to suppress into the normal range defined by our healthy subjects in all patients with active disease; nadir GH determined by IRMA ranged from 0.33-5.0 g/L in this group. In 50% of the active group, nadir GH levels determined by IRMA were less than 1.0 g/L, a GH nadir previously considered normal by strict criteria. When nadir GH levels in the subjects with active disease were measured by polyclonal RIA, there was overlap with the range of RIA values in the healthy subjects. Thus, the IRMA was superior to the RIA in that the overlap between these two groups was eliminated. Subjects with acromegaly in remission included those with normal GH suppression (n ϭ 23; mean nadir GH by IRMA, 0.10 Ϯ 0.006 g/L) and others with abnormal GH suppression by IRMA (n ϭ 15; mean nadir GH by IRMA, 0.35 Ϯ 0.07 g/L). The latter group may have persistent GH dysregulation detected by the sensitive IRMA. GH levels measured by enzyme-linked immunosorbent assay confirmed the IRMA results. IGFBP-3 levels were significantly higher in subjects with active acromegaly (4940 Ϯ 301 g/L) vs. those in healthy subjects (2887 Ϯ 153 g/L; P Ͻ 0.0001) and those in the subjects in remission (2966 g/L; P Ͻ 0.0001). IGFBP-3 levels correlated overall with IGF-I levels (r ϭ 0.765; P Ͻ 0.0001), but IGFBP-3 levels were not predictive of disease status because 32% of the subjects with active acromegaly had normal IGFBP-3 levels. In addition, failure of GH to suppress adequately was not associated with a higher IGFBP-3 level among the subjects in remission.These data indicate that the IRMA is superior to the RIA in disting...

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Oral Glucose Inhibits Growth Hormone Secretion Induced by Human Pancreatic Growth Hormone Releasing Factor 1–44 in Normal Man

Cited by 49 publications

References 14 publications

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Glucose-Dependent Insulinotropic Polypeptide Induced Growth Hormone Secretion in Acromegaly

Evaluation of Disease Status with Sensitive Measures of Growth Hormone Secretion in 60 Postoperative Patients with Acromegaly¹

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Oral Glucose Inhibits Growth Hormone Secretion Induced by Human Pancreatic Growth Hormone Releasing Factor 1–44 in Normal Man

Cited by 49 publications

References 14 publications

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Acute hyperglycemia and activation of the beta-adrenergic system exhibit synergistic inhibitory actions on growth hormone (GH) releasing hormone-induced GH release

Glucose-Dependent Insulinotropic Polypeptide Induced Growth Hormone Secretion in Acromegaly

Evaluation of Disease Status with Sensitive Measures of Growth Hormone Secretion in 60 Postoperative Patients with Acromegaly1

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Evaluation of Disease Status with Sensitive Measures of Growth Hormone Secretion in 60 Postoperative Patients with Acromegaly¹