, Volume 14, Issue 1, pp 79–86 | Cite as

Growth hormone/insulin-like growth factor1 response to acute and chronic growth hormone-releasing peptide-2, growth hormone-releasing hormone 1–44 NH2 and in combination in older men and women with decreased growth hormone secretion



To better appreciate the interactions of GHRP-2 and GHRH 1-44NH2 on the release of GH in normal adult men and women with decreased GH secretion and low serum IGF-1 levels, a series of acute and chronic studies have been performed (n=5 men, 5 women). The acute iv bolus GH responses of these subjects to the two peptides alone and together suggest that the decreased GH secretion may be primarily due to a deficiency of the natural endogenous GHRP, ghrelin, rather than a decreased secretion of endogenous GHRH or excess secretion of SRIF. To determine whether the low GH response to GHRH was due to a limited capacity of pituitary to release GH, higher dosages of GHRP-2 alone were administered. At a dose of 1 μg/kg GHRP-2 the GH response was essentially the same as that elicited by 1 μg/kg GHRH+0.1μg/kg GHRP-2 while the GH response to 10 μg/kg GHRP-2 sc was about twice as high in both men and women. Although these subjects have a limited pituitary capacity to release GH, which is also an indication of decreased GH secretion in the presence of low serum IGF-1 levels, this alone would not explain the low GH response to GHRH. Furthermore, the finding that a low dose of 0.1 μg/kg GHRP-2 augments the GH response to 1 μg/kg GHRH is strongly against an excess secretion of SRIF. Twenty-four hour profiles of GH secretion during placebo, GHRP-2, and various doses of GHRH alone and together with GHRP-2 were studied. In addition, 1 μg/kg/h GHRP-2 was infused continuously sc to these subjects for 30 d. The normal pulsatile secretion of GH as well as the serum IGF-1 level was increased after 24 h and remained elevated for 30 d. With a deficiency of endogenous GHRH, the GH response of GHRP-2 would be little to none, while in subjects with a deficiency of the natural GHRP, the GH response to GHRH would be more attenuated. Thus, in chronic deficiency the GH response would be expected to depend on the degree of the capacity of the pituitary to release GH as well as the type(s) of hormonal deficiency.

Key Words

GHRP-2 GHRH continuous infusion GH pathophysiology decreased GH and IGF-1 normal elderly 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Howard A. D., Feighner, S. D., Cully, D. F., et al. (1996). Science 273, 974–977.PubMedCrossRefGoogle Scholar
  2. 2.
    Dickson, S. L. and Luckman, S. M. (1997). Endocrinology 138, 771–777.PubMedCrossRefGoogle Scholar
  3. 3.
    Bennett, P. A., Thomas, G. B., Howard, A. D., Van der Ploeg, L. H. T., Smith R. G., and Robinson, I. C. A. F. (1997), Endocrinology 138, 4552–4557.PubMedCrossRefGoogle Scholar
  4. 4.
    Kojima, M., Hosada, H., Date, Y., Nakazato, M., Matsu, H., and Kangawa, K. (1999). Nature 402, 656–660.PubMedCrossRefGoogle Scholar
  5. 5.
    Bowers, C. Y. (1998). Cell Mol. Life Sci. 54, 1316–1329.PubMedCrossRefGoogle Scholar
  6. 6.
    Locatelli, V., Grilli, R., Torsello, A., Cella, S. G., Wehrenberg, W. B., and Muller, E. E. (1994). Pediatr. Res. 36, 169–174.PubMedCrossRefGoogle Scholar
  7. 7.
    Cheng, K., Chan, W. W. S., Barreto, A., Convey, E. M., and Smith, R. G. (1989). Endocrinology 124, 2791–2798.PubMedCrossRefGoogle Scholar
  8. 8.
    Bowers, C. Y., Veeraragavan, K., Sethumadahavan, K. (1994). In: Growth hormone II: basic and clinical aspects. Bercu, B. and Walker, R. (eds.) Springer-Verlag: New York.Google Scholar
  9. 9.
    Ghigo, E., Gianotti, L., Arvat, E., Ramunni, J., Valetto, M. R., Broglio, F., Rolla, M., Cavagnini, F., and Muller, E. E. (1999). J. Clin. Endocrinol. Metab. 84, 285–290.PubMedCrossRefGoogle Scholar
  10. 10.
    Jaffe, C. A., Ho, P. J., Demott-Friberg, R., Bowers, C. Y., and Barkan, A. L. (1993). J. Clin. Endocrinol. Metab. 77, 1641–1647.PubMedCrossRefGoogle Scholar

Copyright information

© Human Press Inc 2001

Authors and Affiliations

  1. 1.Tulane University Health Science CenterNew Orleans

Personalised recommendations