TY - JOUR
T1 - Growth hormone/insulin-like growth factor-1 response to acute and chronic growth hormone-releasing peptide-2, growth hormone-releasing hormone 1-44NH2 and in combination in older men and women with decreased growth hormone secretion
AU - Bowers, C. Y.
AU - Granda-Ayala, R.
N1 - Funding Information:
Statistical analyses were performed with SigmaStat for Science (SPSS, Chicago, IL). Data were analyzed by repeated measure analysis of variance (ANOVA) using a general linear model and multiple pairwise comparisons. GH peak, AUC, and IGF-1 levels within and between analyses were measured by within and between subject two-way ANOVA. Mean AUC was determined by the trapezoidal rule. Data are recorded as the mean ± SEM. Acknowledgments We gratefully acknowledge the technicians and fellows of the Endocrinology and Metabolism Section of the Department of Medicine and Robin Alexander for typing the manuscript. We also wish to thank Dr. Fred Wagner at BioNebraska for supplying GHRH 1-44NH2 and Kaken Pharmaceutical Company for the GHRP-2. This work was supported in part by National Institutes of Health grant PHS RR05096-09 (GCRC).
PY - 2001
Y1 - 2001
N2 - 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 + 0.1 μg/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.
AB - 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 + 0.1 μg/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.
KW - Continuous infusion
KW - Decreased GH and IGF-1
KW - GH pathophysiology
KW - GHRH
KW - GHRP-2
KW - Normal elderly
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M3 - Article
C2 - 11322505
AN - SCOPUS:0035079802
SN - 1355-008X
VL - 14
SP - 79
EP - 86
JO - Endocrine
JF - Endocrine
IS - 1
ER -