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Intracellular Glucopenia Causes Prolactin Release in Man

Intracellular Glucopenia Causes Prolactin Release in Man Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in the effective glucose concentration on PRL secretion and looked for an insulin action which was independent of hypoglycemia. The iv administration of insulin (0.1 U/kg)to 12 healthy subjects increased plasma radioimmunoassayable prolactin from 7.9 ± 0.8 (mean ± SE) to 44.8 ±11.3 ng/ml (568% increase, P < 0.005) at 60 min, while plasma glucose decreased from 94.8 ± 4.1 to 34.8 ± 3.3 mg/dl at 20 min. That this response was due to hypoglycemia per se and not th,e fall in blood glucose was shown by the fact that PRL remained unchanged during the rapid decrease in glucose from elevated levels (278 ± 16.7 mg/dl) induced by a glucose bolus (25 g) and 60–min glucose infusion (40–80 g) prior to the start of the study. The effects of intracellular glucopenia which are independent of insulin were studied by infusing 2-deoxy-D-glucose (2DG, 50 mg/kg over 20 min) into 6 normal men. PRL increased from 11.5 ± 2.1 to 33.0 ± 8.6 ng/ml at 60 min (P < 0.05), while glucoserose from 76.4 ± 5.2 to 142.8 ± 10.9 mg/dl by 120 min (P< 0.002). The role of the sympathetic nervous system in this response was determined by the administration of 2DG to 2 bilaterally adrenalectomized and to 2 functionally sympathectomized patients who had had C 5–6 spinal cord transections. The PRL response was normal in the former (16.8 to 43 ng/ml) but exaggerated in the latter (9.6 to 64.8 ng/ml). To determine if insulin had a directeffect which was not mediated by hypoglycemia, 8 normal subjects had insulin (0.1 U/kg) infused over 1 h with enough glucose to prevent hypoglycemia. PRL remained unchanged whilethe maximal glucose change was an increase of 21.1 ± 13.2 mg/dl. Stimulation of endogenous insulin secretion by oral glucose (100 g) in 7 subjects resulted in a nonsignificant decrease in PRL. We conclude that: 1) intracellular glucopenia per se and not other insulineffects release PRL, 2) PRL is released in response to hypoglycemia and not the fall in glucose, and 3) this response is not mediated by peripheral catecholamines since patients with impaired catecholamine secretion have normal or exaggerated PRL release. This content is only available as a PDF. Copyright © 1977 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Clinical Endocrinology and Metabolism Oxford University Press

Intracellular Glucopenia Causes Prolactin Release in Man

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References (16)

Publisher
Oxford University Press
Copyright
Copyright © 1977 by The Endocrine Society
ISSN
0021-972X
eISSN
1945-7197
DOI
10.1210/jcem-45-3-377
Publisher site
See Article on Publisher Site

Abstract

Although it has been known for many years that insulin-induced hypoglycemia causes growth hormone (GH) and cortisol secretion in man, its effects on prolactin (PRL) secretion have been variable. Consequently, we investigated the effects of alteration in the effective glucose concentration on PRL secretion and looked for an insulin action which was independent of hypoglycemia. The iv administration of insulin (0.1 U/kg)to 12 healthy subjects increased plasma radioimmunoassayable prolactin from 7.9 ± 0.8 (mean ± SE) to 44.8 ±11.3 ng/ml (568% increase, P < 0.005) at 60 min, while plasma glucose decreased from 94.8 ± 4.1 to 34.8 ± 3.3 mg/dl at 20 min. That this response was due to hypoglycemia per se and not th,e fall in blood glucose was shown by the fact that PRL remained unchanged during the rapid decrease in glucose from elevated levels (278 ± 16.7 mg/dl) induced by a glucose bolus (25 g) and 60–min glucose infusion (40–80 g) prior to the start of the study. The effects of intracellular glucopenia which are independent of insulin were studied by infusing 2-deoxy-D-glucose (2DG, 50 mg/kg over 20 min) into 6 normal men. PRL increased from 11.5 ± 2.1 to 33.0 ± 8.6 ng/ml at 60 min (P < 0.05), while glucoserose from 76.4 ± 5.2 to 142.8 ± 10.9 mg/dl by 120 min (P< 0.002). The role of the sympathetic nervous system in this response was determined by the administration of 2DG to 2 bilaterally adrenalectomized and to 2 functionally sympathectomized patients who had had C 5–6 spinal cord transections. The PRL response was normal in the former (16.8 to 43 ng/ml) but exaggerated in the latter (9.6 to 64.8 ng/ml). To determine if insulin had a directeffect which was not mediated by hypoglycemia, 8 normal subjects had insulin (0.1 U/kg) infused over 1 h with enough glucose to prevent hypoglycemia. PRL remained unchanged whilethe maximal glucose change was an increase of 21.1 ± 13.2 mg/dl. Stimulation of endogenous insulin secretion by oral glucose (100 g) in 7 subjects resulted in a nonsignificant decrease in PRL. We conclude that: 1) intracellular glucopenia per se and not other insulineffects release PRL, 2) PRL is released in response to hypoglycemia and not the fall in glucose, and 3) this response is not mediated by peripheral catecholamines since patients with impaired catecholamine secretion have normal or exaggerated PRL release. This content is only available as a PDF. Copyright © 1977 by The Endocrine Society

Journal

Journal of Clinical Endocrinology and Metabolism – Oxford University Press

Published: Sep 1, 1977

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