scholarly journals Different Responses of Bone Alkaline Phosphatase Isoforms During Recombinant Insulin-like Growth Factor-I (IGF-I) and During Growth Hormone Therapy in Adults with Growth Hormone Deficiency

1997 ◽  
Vol 12 (2) ◽  
pp. 210-220 ◽  
Author(s):  
Per Magnusson ◽  
Marie Degerblad ◽  
Maria Sääf ◽  
Lasse Larsson ◽  
Marja Thorén
2018 ◽  
Vol 65 (2) ◽  
Author(s):  
Ewelina Witkowska-Sędek ◽  
Anna Stelmaszczyk-Emmel ◽  
Anna Majcher ◽  
Urszula Demkow ◽  
Beata Pyrżak

The relationships between bone turnover, the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis and vitamin D are complex, but still not fully explained. The GH/IGF-1 axis and vitamin D could modulate their metabolism mutually and influence activation of cell proliferation, maturation, and mineralization as well as bone resorption. The aim of this study was to evaluate the reciprocal associations between bone formation markers [alkaline phosphatase (ALP), bone alkaline phosphatase (BALP)], the GH/IGF-1 axis and 25-hydroxyvitamin D [25(OH)D] in children with growth hormone deficiency at baseline and during recombinant human growth hormone (rhGH) therapy. ALP, BALP, 25(OH)D and IGF-1 concentrations were evaluated in 53 patients included in this prospective three-year study. ALP, BALP and IGF-1 increased during rhGH therapy. Baseline ALP correlated positively with baseline height velocity (HV). ALP and BALP at 12 months correlated positively with HV in the first year of therapy. We found positive correlations between ALP and IGF-1 at baseline and during the first year of therapy, between BALP at 12 months and rhGH dose in the first year of therapy, and between mean doses of cholecalciferol in the first year of rhGH therapy and early changes in BALP during rhGH therapy. Our results indicate that vitamin D supplementation enhances the effect of rhGH on bone formation activity, which could improve the effects of rhGH therapy. ALP and BALP are useful in early prediction of the effects of rhGH therapy, but their utility as long-term predictors is not sufficient. 


2005 ◽  
Vol 63 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Rikke Beck Jensen ◽  
Katrine Arp Jeppesen ◽  
Signe Vielwerth ◽  
Kim Fleischer Michaelsen ◽  
Katharina M. Main ◽  
...  

1993 ◽  
Vol 40 (2) ◽  
pp. 185-190 ◽  
Author(s):  
YUKIHIRO HASEGAWA ◽  
TOMONOBU HASEGAWA ◽  
TAIJI ASO ◽  
SHINOBU KOTOH ◽  
YUTAKA TSUCHIYA ◽  
...  

1992 ◽  
Vol 127 (4) ◽  
pp. 351-358 ◽  
Author(s):  
Zvi Laron ◽  
Anne-Maria Suikkari ◽  
Beatrice Klinger ◽  
Aviva Silbergeld ◽  
Athalia Pertzelan ◽  
...  

Insulin-like growth factors (IGFs) mediate the effects of growth hormone (GH), and the insulin-like growth factor-binding proteins (IGFBPs) modulate the actions of IGFs in tissues. We studied the circulating levels of IGFBP-1 in 6 children and 9 adults with Laron type dwarfism (LTD), in 11 children and 21 adults with growth hormone deficiency (GHD), and in 8 children with constitutional short stature. Compared with the situation in healthy children, the basal serum IGFBP-1 concentration was 5.4-fold higher in LTD children, 4.1-fold higher in GHD children, and 3.8-fold higher in children with short stature (p<0.02 vs controls in all groups). In adult patients with multiple pituitary hormone deficiency (MPHD), the IGFBP-1 concentration was 2-fold elevated, but it was normal in adult LTD patients. Intravenous (N= 10) or subcutaneous (N=9) administration ofIGF-I (75 μg·kg−1 and 150 μg·kg−1, respectively) in LTD children resulted in a rapid 50–60% fall in serum insulin (p<0.02), a decline in blood glucose and a concomitant 40–60% rise of IGFBP-1 levels (p<0.05). Treatment for seven days with IGF-I (150 μg·kg−1·d−1) resulted in a decrease by 34% and 44% of serum IGFBP-1 level in two out of three children with LTD. After prolonged GH therapy, the IGFBP-1 level fell in GHD children by 29% (p<0.05), in GHD adults by 52% (p<0.02) and in children with constitutional short stature by 17% (p<0.02). IGFBP-1 and insulin concentrations were inversely related in patients with GHD (r= −0.66, p<0.001) or with LTD (r= −0.57, p<0.05). Our data suggest that: (a) increased IGFBP-1 concentration in LTD, GHD and constitutional short children may, at least in part, be accounted for by an IGF-I deficiency; (b) both the rise in IGF-I and a fall in insulin contributed to the rise in IGFBP-1 after acute IGF-I administration; (c) prolonged IGF-I or GH treatment causes a persistent decline in IGFBP-1 concentration. In conclusion, IGF-I and GH may regulate IGFBP-1 secretion either directly or via insulin.


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