Hypothalamic Regulation of Growth Hormone Secretion

Abrams, Robert L.; Parker, Mary L.; Blanco, Santander; Reichlin, Seymour; Daughaday, William H.

doi:10.1210/endo-78-3-605

Cited by 94 publications

(23 citation statements)

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“…During insulin hypoglycemia the inhibitory effect of alpha blockade on growth hormone secretion was pronounced while the stimulatory effect of beta blockade was less impressive and was associated with more prolonged hypoglycemia and lower plasma FFA concentrations. More prolonged hypoglycemia probably was not responsible for the enhanced HGH response during beta blockade as studies in monkeys during insulin hypoglycemia have shown that growth hormone hypersecretion occurs while blood glucose concentrations are falling but return to normal even though plasma glucose concentrations remain depressed (30). Limited data on the effect of plasma FFA on growth hormone levels are available.…”

Section: Resultsmentioning

confidence: 99%

Adrenergic receptor control mechanism for growth hormone secretion

Blackard¹,

Heidingsfelder²

1968

J. Clin. Invest.

268

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A B S T R A C T The influence of catecholamines on growth hormone secretion has been difficult to establish previously, possibly because of the suppressive effect of the induced hyperglycemia on growth hormone concentrations. In this study, an adrenergic receptor control mechanism for human growth hormone (HGH) secretion was uncovered by studying the effects of alpha and beta receptor blockade on insulin-induced growth hormone elevations in volunteer subjects.Alpha adrenergic blockade with phentolamine during insulin hypoglycemia, 0.1 U/kg, inhibited growth hormon elevations to 30-50% of values in the same subjects during insulin hypoglycemia without adrenergic blockade. More complete inhibition by phentolamine could not be demonstrated at a lower dose of insulin (0.05 U/kg). Beta adrenergic blockade with propranolol during insulin hypoglycemia significantly enhanced HGH concentrations in paired experiments. The inhibiting effect of alpha adrenergic receptor blockade on HGH concentrations could not be attributed to differences in blood glucose or free fatty acid values; however, more prolonged hypoglycemia and lower plasma free fatty acid values may have been a factor in the greater HGH concentrations observed during beta blockade. In the absence of insulin induced hypoglycemia, neither alpha nor beta adrenergic receptor blockade had a detectable

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Section: Resultsmentioning

confidence: 99%

Adrenergic receptor control mechanism for growth hormone secretion

Blackard¹,

Heidingsfelder²

1968

J. Clin. Invest.

268

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“…Autoregulation of adrenocorticotropic hormone (ACTH) was first suggested by the observations of Gemzell and Heijkenskjold (30), Kitay, Holub, and Jailer (31), and Hodges and Vernikos (32). Characterization of this type of control mechanism for ACTH was described by Motta, Mangili, and Martini in 1965 (33 (40) and, in man, after pituitary stalk section (41,42) or hypothalamic disease (43,44). Also, microinjection of glucose into the hypothalamus, coincident with systemic hypoglycemia, prevents the normal GH response to hypoglycemia (45).…”

Section: Discussionmentioning

confidence: 99%

The effect of administration of human growth hormone on the plasma growth hormone, cortisol, glucose, and free fatty acid response to insulin: evidence for growth hormone autoregulation in man

Abrams¹,

Grumbach²,

Kaplan³

1971

J. Clin. Invest.

Self Cite

125

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A B S T R A C T The effect of administration of human growth hormone (HGH) (3 mg every 6 hr for 6 days) on the endogenous GH response to insulin-induced hypoglycemia at 8, 12, 24, and 48 hr posttreatment was studied in 11 healthy male adults. Free fatty acid, cortisol, and glucose responses pre-and posttreatment with HGH were evaluated concurrently. Control subjects received saline injections to evaluate relationship of GH responses to the periodicity of insulin tolerance tests. The data were compared for each subject pre-and posttreatment with HGH as well as by comparison of the results of the saline-treated group with those of the HGH-treated group.The mean maximal GH concentration in response to insulin-induced hypoglycemia for all the subjects (n = 16) was 31.1 ±3.6 ng/ml (+SEM) on day 1 of the control period and 23.4 ±3.1 (SEM) on day 2, not statistically significant.A significant decrease in the maximal peak GH response (n = 8) after insulin-induced hypoglycemia was observed at 8 and 12 hr after HGH administration was terminated with mean peak values for GH of 4.6 +1.3 ng/ml and 10.4 +1.9 ng/ml, respectively (P < 0.01). A progressive return to control values was noted between 12 and 24 hr. The GH responsiveness of the saline-treated group (n = 5) was unchanged from that observed during the control period.The fasting glucose values were unchanged in the GH-treated group from those of the control period or of the saline-treated controls. Insulin resistance was ap-

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“…The observation that the intravenous injection of insulin into control subjects results in rapid elevations of plasma cortisol (4,5) and growth hormone (6)(7)(8)(9) also supports the possible physiologic importance of these hormones as insulin antagonists. Since the release of these two hormones depends on adequate hypothalamic as well as pituitary and adrenal function (5,7,10), it was apparent that a rapid test of both the hypothalamo-pituitary-adrenal axis for the secretion of cortisol and the hypothalamo-pituitary axis for the secretion of growth hormone could be developed with insulininduced hypoglycemia as a stimulus.…”

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confidence: 99%