Prevention of<scp>l</scp>-Dopa-Induced Growth Hormone Stimulation by Hyperglycemia

Mims, Robert B.; Scott, Cranford L.; Modebe, O; Bethune, John E.

doi:10.1210/jcem-37-5-660

Cited by 36 publications

(13 citation statements)

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“…Hypoglycemia elicits a reflex GH discharge, and glucose administration is able to block GH under different circumstances. Though acute hyperglycemia blocks GH secre tion elicited by arginine, exercise and ¿-dopa [2][3][4], the glucose blockade is either transient or selective. In fact, acute hypergly cemia does not alter GH secretion stimulated by sleep, stress, or pyrogen administration [10][11][12], and in some subjects it is un able to reduce arginine-induced GH release [13].…”

Section: Discussionmentioning

confidence: 99%

Activation of Cholinergic Neurotransmission by Pyridostigmine Reverses the Inhibitory Effect of Hyperglycemia on Growth Hormone (GH) Releasing Hormone-Induced GH Secretion in Man: Does Acute Hyperglycemia Act through Hypothalamic Release of Somatostatin?

Peñalva¹,

Burguera²,

Casabiell³

et al. 1989

Neuroendocrinology

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Acute hyperglycemia blocks growth hormone (GH) secretion in response to provocative stimuli including growth hormone releasing hormone (GHRH) administration. However, the precise mechanism of glucose action is unknown. To determine if enhanced somatostatinergic stimulation accounts for the decreased GH secretion, we studied the effect of enhanced cholinergic tone by pyridostigmine on the hyperglycemia blockade of GH release in 7 normal subjects. Pyridostigmine, an acetylcholin-esterase inhibitor, has been postulated as an inhibitor of somatostatin release. Each subject underwent 4 tests with GHRH injection (100 µg i.v. at 0 min). In the first (control) test, placebo was administered before GHRH. In the second test, 100 g of glucose was administered p.o. 45 min before GHRH. In the third test, pyridostigmine, 120 mg p.o., was administered 60 min before GHRH, and in the fourth test, pyridostigmine, glucose and GHRH were administered at -60, -45 and 0 min, respectively. GHRH-induced GH secretion of 25.8 ± 4.5 ng/ml was significantly reduced by previous glucose administration (12.1 ± 4.5 ng/ml) and significantly potentiated by previous pyridostigmine pretreatment (56.5 ± 16.8 ng/ml). In the fourth test (pyridostigmine plus glucose plus GHRH) the GH peak of 42.4 ± 9.2 ng/ml was significantly higher than after GHRH alone and not different to the pyridostigmine-GHRH test. In conclusion, central cholinergic activation by pyridostigmine reversed the hyperglycemic blockade of GHRH-induced GH secretion. In addition, hyperglycemia was unable to reduce the potentiating effect of pyridostigmine on GH secretion elicited by GHRH. Based on the reported actions of pyridostigmine, acute hyperglycemia might act over GH release by inducing hypothalamic somatostatin release.

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Section: Discussionmentioning

confidence: 99%

Activation of Cholinergic Neurotransmission by Pyridostigmine Reverses the Inhibitory Effect of Hyperglycemia on Growth Hormone (GH) Releasing Hormone-Induced GH Secretion in Man: Does Acute Hyperglycemia Act through Hypothalamic Release of Somatostatin?

Peñalva¹,

Burguera²,

Casabiell³

et al. 1989

Neuroendocrinology

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“…Direct experimental evidence for this hypothesis is the lack of Glc effect on GH and thyrotropin release from rat pituitary cells in vitro (8) and the inverse relationship between Glc concentration and SRIH release from rat hypothalamic cells in vitro (9,10). The clinical counterpart of this experimental evidence is Glc-induced block of GH response to stimuli acting at the suprapituitary level, such as arginine (11), exercise (12) and L-DOPA (13). All these data seem to imply that the action of Glc on GH release is exerted by a stimulation of hypothalamic SRIH.…”

Section: Discussionmentioning

confidence: 99%

Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics

Attanasio

Oppizzi

Lodrini

et al. 1999

European Journal of Endocrinology

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Objective and design: A decrease of GH levels below 2 mg/l after an oral glucose tolerance test (OGTT) is still currently accepted as the gold standard for assessing cure in surgically treated acromegaly. Whether glucose-induced suppression of GH is accompanied by a restoration of normal GH late rebound has not yet been evaluated in this disease. In order to assess the restoration of normal GH regulation after removal of a pituitary adenoma, we have evaluated GH changes after an OGTT in a series of selected acromegalic patients (transsphenoidal surgery and lack of pituitary failure). Methods: Twenty-nine patients (13 male, 16 female, age range 27-70 years) entered the study. Their neuroradiological imaging before neurosurgery showed microadenoma in 7, intrasellar macroadenoma in 8 and macroadenoma with extrasellar extension in 14. Plasma GH levels were assayed up to 300 min after glucose administration (75 g p.o.) and IGF-I on basal samples. Results: Basal GH levels were below 5 mg/l in 20 patients and below 2 mg/l in 5 of these. Normal ageadjusted IGF-I levels were observed in 12 patients. GH values were suppressed below 2 mg/l during an OGTT in 13 patients, and below 1 mg/l in 7 of these. In 9 patients out of these 13, a marked rise in GH levels occurred after nadir. Baseline and nadir GH values of these 9 patients were not different from the corresponding values of the other 4 patients without OGTT-induced late GH peaks. Conclusions: GH rebound after GH nadir occurs in acromegalic patients considered as cured on the basis of OGTT-induced GH suppression and/or IGF-I normalization. The restoration of this physiological response could be regarded as a marker of recovered/preserved integrity of the hypothalamic-pituitary axis. Even though the reason for this GH rebound has not yet been elucidated (GHRH discharge?/end of somatostatin inhibition?), the lack of late GH peak in the patients regarded as cured by the usual criteria could be due to injury to the pituitary stalk caused by the adenoma or by surgical manipulation.

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“…of the growth hormone response to L-dopa in normals during simultaneous intravenous glucose administration. 4 Of interest in their study was the prevailing glucose concentration of approximately 180 mg./lOO ml. during the sixty-to-ninety-minute period following L-dopa administration.…”

Section: Discussionmentioning

confidence: 99%

“…8 Furthermore, the utility of L-dopa as a provocative agent in the measurement of growth hormone reserve in diabetics is not established, and studies in this regard are limited. 4 We have studied the growth hormone response to L-dopa in a group of insulin-dependent diabetics and in a normal group that was rechallenged with L-dopa while hyperglycemic. It is the purpose of this communication to report the results of these studies.…”

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confidence: 99%

Effect of Glucose on the Growth Hormone Response to L-dopa in Normal and Diabetic Subjects

1975

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The effect of hyperglycemia on the growth hormone response to oral L-dopa (500 mg.) was assessed in eight normal and eight insulin-dependent diabetic subjects. A peak growth hormone response of 21.0 +/- 4.0 ng./ml. (mean +/- S.E.M.), significantly above baseline (p less than 0.01), was achieved in the normal group following oral L-dopa. Glucose concentrations did not change and were approximately 80 mg./100 ml. throughout. Administration of 100 gm. oral glucose with the L-dopa, or thirty minutes thereafter, totally suppressed the growth hormone response in all eight and six of the subjects, respectively. A peak growth hormone response of 20.0 "/- 1.7 ng./ml. (mean +/- S.E.M.), significantly above baseline (p less than 0.001), was obtained in eight nonobese, insulin-dependent diabetics, in spite of prevailing hyperglycemia (mean plasma glucose 243-258 mg./100 ml.) throughout the test. Endogenous hyperglycemia was achieved in these patients by lessening the usual strict adherence to plasma glucose control for the purpose of the study. These results suggest an abnormality in the hypothalamus or pituitary of diabetic subjects allowing growth hormone responsiveness in spite of hyperglycemia.

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Prevention ofl-Dopa-Induced Growth Hormone Stimulation by Hyperglycemia

Cited by 36 publications

References 0 publications

Activation of Cholinergic Neurotransmission by Pyridostigmine Reverses the Inhibitory Effect of Hyperglycemia on Growth Hormone (GH) Releasing Hormone-Induced GH Secretion in Man: Does Acute Hyperglycemia Act through Hypothalamic Release of Somatostatin?

Activation of Cholinergic Neurotransmission by Pyridostigmine Reverses the Inhibitory Effect of Hyperglycemia on Growth Hormone (GH) Releasing Hormone-Induced GH Secretion in Man: Does Acute Hyperglycemia Act through Hypothalamic Release of Somatostatin?

Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics

Effect of Glucose on the Growth Hormone Response to L-dopa in Normal and Diabetic Subjects

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