The effect of growth hormone replacement in adult growth hormone deficiency on the diurnal and ultradian dynamics of ghrelin, leptin, soluble leptin receptor and adiponectin

2005 ◽  
Vol 113 (S 1) ◽  
Author(s):  
F Joseph ◽  
G Brabant ◽  
A Ahmad ◽  
W Fraser ◽  
J Vora
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Leptin Receptor ◽  
Hormone Replacement ◽  
Hormone Deficiency ◽  
Growth Hormone Replacement ◽  
Adult Growth Hormone Deficiency ◽  
Adult Growth ◽  
Soluble Leptin Receptor

Parathyroid responsiveness to hypocalcemic and hypercalcemic stimuli in adult growth hormone deficiency after growth hormone replacement

2004 ◽  
Vol 286 (6) ◽  
pp. E986-E993 ◽  
Author(s):  
Aftab M. Ahmad ◽  
Marion T. Hopkins ◽  
Joegi Thomas ◽  
Brian H. Durham ◽  
William D. Fraser ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Parathyroid Gland ◽  
Calcium Concentration ◽  
Hormone Replacement ◽  
Hormone Deficiency ◽  
Growth Hormone Replacement ◽  
Adult Growth Hormone Deficiency ◽  
Gh Replacement ◽  
Adult Growth

Adult growth hormone deficiency (AGHD) is associated with osteoporosis. Previous reports have suggested that alterations in parathyroid gland responsiveness to changes in calcium concentration may play a role in the genesis of osteoporosis in untreated AGHD patients. We investigated the endogenous parathyroid hormone [PTH-(1–84)] response to hypocalcemic and hypercalcemic stimuli induced by sodium EDTA and calcium gluconate infusion, respectively, and to PTH-(1–34) infusion in AGHD patients before and during GH replacement (GHR). We have demonstrated that the maximum PTH-(1–84) stimulation and suppression occurred at significantly higher calcium concentrations and in response to smaller changes in calcium concentrations after GHR. The calcemic response to the effects of PTH-(1–34) infusion significantly increased after GHR. The calcium set point (the calcium concentration at which the rate of PTH secretion is one-half of its maximal value) significantly increased in all groups after 3 mo on GHR, and it increased further at 12 mo. Our results suggest increased parathyroid gland sensitivity to smaller changes in serum calcium and increased end-organ sensitivity to the effects of PTH in AGHD patients after GHR. These findings may help us to understand the mechanisms underlying the genesis of osteoporosis in AGHD patients.

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