scholarly journals Consequences of lifetime isolated growth hormone (GH) deficiency and effects of short-term GH treatment on bone in adults with a mutation in the GHRH-receptor gene

2009 ◽  
Vol 70 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Francisco J. A. de Paula ◽  
Miburge B. Góis-Júnior ◽  
Manuel H. Aguiar-Oliveira ◽  
Francisco de A. Pereira ◽  
Carla R. P. Oliveira ◽  
...  
Endocrine ◽  
2021 ◽  
Author(s):  
Manuela A. Melo ◽  
Lysandro P. Borges ◽  
Roberto Salvatori ◽  
Daniela R. V. Souza ◽  
Hertz T. Santos-Júnior ◽  
...  

2006 ◽  
Vol 65 (4) ◽  
pp. 423-428 ◽  
Author(s):  
F. Brandou ◽  
I. Aloulou ◽  
A. Razimbaud ◽  
C. Fédou ◽  
J. Mercier ◽  
...  

2008 ◽  
Vol 32 (3) ◽  
pp. 380-392 ◽  
Author(s):  
Scott A. Gahr ◽  
Roger L. Vallejo ◽  
Gregory M. Weber ◽  
Brian S. Shepherd ◽  
Jeffrey T. Silverstein ◽  
...  

Although studies have established that exogenous growth hormone (GH) treatment stimulates growth in fish, its effects on target tissue gene expression are not well characterized. We assessed the effects of Posilac (Monsanto, St. Louis, MO), a recombinant bovine GH, on tissue transcript levels in rainbow trout selected from two high-growth rate and two low-growth rate families. Transcript abundance was measured in liver and muscle with the Genome Research in Atlantic Salmon Project (GRASP) 16K cDNA microarray. A selection of the genes identified as altered by the microarray and transcripts for insulin-like growth factors, growth hormone receptors (GHRs), and myostatins were measured by real-time PCR in the liver, muscle, brain, kidney, intestine, stomach, gill, and heart. In general, transcripts identified as differentially regulated in the muscle on the microarray showed similar directional changes of expression in the other nonhepatic tissues. A total of 114 and 66 transcripts were identified by microarray as differentially expressed with GH treatment across growth rate for muscle and liver, respectively. The largest proportion of these transcripts represented novel transcripts, followed by immune and metabolism-related genes. We have identified a number of genes related to lipid metabolism, supporting a modulation in lipid metabolism following GH treatment. Most notable among the growth-axis genes measured by real-time PCR were increases in GHR1 and -2 transcripts in liver and muscle. Our results indicate that short-term GH treatment activates the immune system, shifts the metabolic sectors, and modulates growth-regulating genes.


1995 ◽  
Vol 38 (3) ◽  
pp. 418-421 ◽  
Author(s):  
Ashraf Kamel ◽  
Véronique Margery ◽  
Gunnar Norstedt ◽  
Marja Thorén ◽  
Anne-Christine Lindgren ◽  
...  

1999 ◽  
Vol 46 (Suppl) ◽  
pp. S35-S38 ◽  
Author(s):  
RYUICHI KUROMARU ◽  
HITOSHI KOHNO ◽  
NAMI UEYAMA ◽  
HASSAN MOHAMED SALAMA HASSAN ◽  
SUNAO HONDA ◽  
...  

2017 ◽  
Vol 88 (3-4) ◽  
pp. 258-264 ◽  
Author(s):  
Dina A. Schott ◽  
Willem J.M. Gerver ◽  
Constance T.R.M. Stumpel

Background/Aims: Kabuki syndrome (KS) is a rare genetic malformation syndrome, resulting in characteristic features such as short stature. We investigate whether growth hormone (GH) treatment increases linear height and influences body proportions in KS children. Methods: In this prospective study, 18 genetically confirmed prepubertal KS children (9 females and 9 males) aged from 3.8 to 10.1 years (mean 6.8 ± 2.1 years) were treated with recombinant human GH (rhGH) for 1 year. Calculations for height, height velocity, BMI, sitting height, and subischial leg length were made. Bone age, insulin-like growth factor (IGF-I), and IGF binding protein 3 (IGFBP-3) were also measured. Results: This study showed an increase in height standard deviation score (SDS) for the whole group from –2.40 to –1.69 (p < 0.05) after 1 year of rhGH treatment. The change in height SDS within 1 year was >0.7 SDS for 10 subjects and >0.5 SDS for 3 subjects. The mean IGF-I SDS at the start of the study was –0.70 (±1.07), which increased after 12 months to 1.41 (±0.91) (p < 0.05). KS children who received rhGH at a younger age displayed significantly greater increases in height than those who started when they were older. The same was true for both gene mutation KMT2D versus KDM6A and for GH deficiency versus non-GH deficiency KS children (p < 0.05). Throughout the course of rhGH treatment, the subjects’ body proportions remained normal. Conclusions: All participants experienced catch-up growth during the year of rhGH treatment, but without an influence on body proportions.


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