Endogenous histamine reduces plasma insulin-like growth factor I via H 1 receptor-mediated pathway in the rat

Endogenous histamine reduces plasma insulin-like growth factor I via H 1 receptor-mediated... Endotoxin has been recently shown to reduce plasma insulin-like growth factor I. As it was reported that histamine can induce gut-derived endotoxemia, we wanted to determine whether histamine has a similar effect on plasma insulin-like growth factor I. Compound 48/80 (a histamine releaser) was injected subcutaneously into rats, then blood was taken for plasma insulin-like growth factor I assay and the livers were assayed for insulin-like growth factor I mRNA. Like endotoxin, injection of compound 48/80 significantly reduced plasma insulin-like growth factor I. Six hours post-injection, plasma insulin-like growth factor I was reduced by 61% ( P <0.001), and 24 h post-injection, it was still lower (by 35% P <0.001) than in the control group. Hepatic insulin-like growth factor I mRNA was not reduced by this treatment. The effect of compound 48/80 on plasma insulin-like growth factor I was significantly attenuated by oral administration of the histamine H 1 receptor antagonist (chlorpheniramine), but not by the histamine H 2 receptor antagonists (cimetidine and ranitidine). Oral administration of polymyxin B (an antiendotoxin antibiotic) did not attenuate the effect of compound 48/80 on plasma insulin-like growth factor I at all. In conclusion, endogenous histamine reduces plasma insulin-like growth factor I via H 1 receptor-mediated pathway. Our study suggests a novel role of histamine in the regulation of insulin-like growth factor I metabolism in vivo. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Pharmacology Elsevier

Endogenous histamine reduces plasma insulin-like growth factor I via H 1 receptor-mediated pathway in the rat

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Publisher
Elsevier
Copyright
Copyright © 1999 Elsevier Science B.V.
ISSN
0014-2999
D.O.I.
10.1016/S0014-2999(99)00309-X
Publisher site
See Article on Publisher Site

Abstract

Endotoxin has been recently shown to reduce plasma insulin-like growth factor I. As it was reported that histamine can induce gut-derived endotoxemia, we wanted to determine whether histamine has a similar effect on plasma insulin-like growth factor I. Compound 48/80 (a histamine releaser) was injected subcutaneously into rats, then blood was taken for plasma insulin-like growth factor I assay and the livers were assayed for insulin-like growth factor I mRNA. Like endotoxin, injection of compound 48/80 significantly reduced plasma insulin-like growth factor I. Six hours post-injection, plasma insulin-like growth factor I was reduced by 61% ( P <0.001), and 24 h post-injection, it was still lower (by 35% P <0.001) than in the control group. Hepatic insulin-like growth factor I mRNA was not reduced by this treatment. The effect of compound 48/80 on plasma insulin-like growth factor I was significantly attenuated by oral administration of the histamine H 1 receptor antagonist (chlorpheniramine), but not by the histamine H 2 receptor antagonists (cimetidine and ranitidine). Oral administration of polymyxin B (an antiendotoxin antibiotic) did not attenuate the effect of compound 48/80 on plasma insulin-like growth factor I at all. In conclusion, endogenous histamine reduces plasma insulin-like growth factor I via H 1 receptor-mediated pathway. Our study suggests a novel role of histamine in the regulation of insulin-like growth factor I metabolism in vivo.

Journal

European Journal of PharmacologyElsevier

Published: Jun 25, 1999

References

  • Insulin-like growth factors and their binding proteins: biological actions
    Jones, J.I; Clemmons, D.R
  • Hepatic production and intestinal uptake of IGF-I: response to infection
    Lang, C.H; Frost, R.A; Ejiofor, J; Lacy, D.B; McGuinness, O.P
  • Growth hormone potentiates the in vivo biological activities of endotoxin in the rat
    Liao, W; Rudling, M; Angelin, B
  • Alterations in the insulin-like growth factor system in trauma patients
    Wojnar, M.M; Fan, J; Frost, R.A; Gelato, M.C; Lang, C.H

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