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Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa.
Biol Psychiatry. 1998 Feb 01; 43(3):181-7.BP

Abstract

BACKGROUND

In anorexia nervosa (AN), growth hormone (GH) hypersecretion and low insulin-like growth factor I (IGF-I) levels are present. It is unclear whether this is due to a peripheral GH resistance and a reduced IGF-I negative feedback on GH secretion or to a primary hypothalamic dysfunction. In AN, in contrast to normal subjects, cholinergic antagonists and agonists, whose action is somatostatin (SS)-mediated, have reduced and absent effects on the GH response to growth hormone-releasing hormone (GHRH). Since arginine, another substance acting via inhibition of SS, maintains its potentiating effect on GH secretion in AN, it has been hypothesized that somewhat specific alteration of the SS-mediated cholinergic influence may be present in this condition. To further clarify the neural control of AH secretion in AN, we evaluated the effects of beta-adrenergic agonists and antagonists, which are known to inhibit and increase, respectively, the GHRH-induced GH secretion in normal subjects.

METHODS

We studied the effect of atenolol (ATE), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-adrenergic agonist, on the GHRH-induced GH release in 10 patients with AN and in 10 normal age-matched women (NW).

RESULTS

Basal GH levels were higher, whereas IGF-I were lower in AN than in NW. The GHRH-induced GH rise in AN was higher than that in NW. ATE significantly enhanced the GH response to GHRH in NW, but not in AN. The GH responses to GHRH after ATE pretreatment were similar in NW and in AN. The GH response to GHRH was inhibited by SALB in both NW and AN. The GH responses to GHRH after SALB pretreatment were similar in NW and AN.

CONCLUSIONS

These data reveal an exaggerated somatotrope responsiveness to GHRH in AN that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairment of beta-adrenergic influence on GH secretion is present in anorexia nervosa.

Authors+Show Affiliations

Department of Internal Medicine, University of Turin, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9494699

Citation

Gianotti, L, et al. "Effects of Beta-adrenergic Agonists and Antagonists On the Growth Hormone Response to Growth Hormone-releasing Hormone in Anorexia Nervosa." Biological Psychiatry, vol. 43, no. 3, 1998, pp. 181-7.
Gianotti L, Arvat E, Valetto MR, et al. Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa. Biol Psychiatry. 1998;43(3):181-7.
Gianotti, L., Arvat, E., Valetto, M. R., Ramunni, J., Di Vito, L., Maccagno, B., Camanni, F., & Ghigo, E. (1998). Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa. Biological Psychiatry, 43(3), 181-7.
Gianotti L, et al. Effects of Beta-adrenergic Agonists and Antagonists On the Growth Hormone Response to Growth Hormone-releasing Hormone in Anorexia Nervosa. Biol Psychiatry. 1998 Feb 1;43(3):181-7. PubMed PMID: 9494699.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa. AU - Gianotti,L, AU - Arvat,E, AU - Valetto,M R, AU - Ramunni,J, AU - Di Vito,L, AU - Maccagno,B, AU - Camanni,F, AU - Ghigo,E, PY - 1998/3/12/pubmed PY - 1998/3/12/medline PY - 1998/3/12/entrez SP - 181 EP - 7 JF - Biological psychiatry JO - Biol. Psychiatry VL - 43 IS - 3 N2 - BACKGROUND: In anorexia nervosa (AN), growth hormone (GH) hypersecretion and low insulin-like growth factor I (IGF-I) levels are present. It is unclear whether this is due to a peripheral GH resistance and a reduced IGF-I negative feedback on GH secretion or to a primary hypothalamic dysfunction. In AN, in contrast to normal subjects, cholinergic antagonists and agonists, whose action is somatostatin (SS)-mediated, have reduced and absent effects on the GH response to growth hormone-releasing hormone (GHRH). Since arginine, another substance acting via inhibition of SS, maintains its potentiating effect on GH secretion in AN, it has been hypothesized that somewhat specific alteration of the SS-mediated cholinergic influence may be present in this condition. To further clarify the neural control of AH secretion in AN, we evaluated the effects of beta-adrenergic agonists and antagonists, which are known to inhibit and increase, respectively, the GHRH-induced GH secretion in normal subjects. METHODS: We studied the effect of atenolol (ATE), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-adrenergic agonist, on the GHRH-induced GH release in 10 patients with AN and in 10 normal age-matched women (NW). RESULTS: Basal GH levels were higher, whereas IGF-I were lower in AN than in NW. The GHRH-induced GH rise in AN was higher than that in NW. ATE significantly enhanced the GH response to GHRH in NW, but not in AN. The GH responses to GHRH after ATE pretreatment were similar in NW and in AN. The GH response to GHRH was inhibited by SALB in both NW and AN. The GH responses to GHRH after SALB pretreatment were similar in NW and AN. CONCLUSIONS: These data reveal an exaggerated somatotrope responsiveness to GHRH in AN that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairment of beta-adrenergic influence on GH secretion is present in anorexia nervosa. SN - 0006-3223 UR - https://www.unboundmedicine.com/medline/citation/9494699/Effects_of_beta_adrenergic_agonists_and_antagonists_on_the_growth_hormone_response_to_growth_hormone_releasing_hormone_in_anorexia_nervosa_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-3223(97)00014-0 DB - PRIME DP - Unbound Medicine ER -