Growth Hormone and Prolactin Receptors in Adipogenesis: STAT-5 Activation, Suppressors of Cytokine Signaling, and Regulation of Insulin-Like Growth Factor I

2006 ◽  
Vol 66 (3) ◽  
pp. 101-110 ◽  
Author(s):  
Don Fleenor ◽  
Ramamani Arumugam ◽  
Michael Freemark
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Cytokine Signaling ◽  
Insulin Like Growth Factor ◽  
Prolactin Receptors ◽  
Factor I ◽  
Suppressors Of Cytokine Signaling ◽  
Growth Factor I

Endotoxin attenuates growth hormone-induced hepatic insulin-like growth factor I expression by inhibiting JAK2/STAT5 signal transduction and STAT5b DNA binding

2007 ◽  
Vol 292 (6) ◽  
pp. E1856-E1862 ◽  
Author(s):  
Yu Chen ◽  
Difei Sun ◽  
Vidya M. R. Krishnamurthy ◽  
Ralph Rabkin
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Janus Kinase ◽  
Cytokine Gene Expression ◽  
Cytokine Signaling ◽  
Insulin Like Growth Factor ◽  
Gh Treatment ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Gram-negative sepsis with release of endotoxin is a frequent cause of cachexia that develops partly because of resistance to growth hormone (GH) with reduced insulin-like growth factor-I (IGF-I) expression. We set out to more fully characterize the mechanisms for the resistance and to determine whether in addition to a defect in the janus kinase 2 (JAK2)-signal transducer and activator of transcription (STAT) 5b pathway, required for GH-induced IGF-I expression, there might also be a more distal defect. Conscious rats were given endotoxin and studied 4 h later. In liver of these animals, GH-induced JAK2 and STAT5 phosphorylation was impaired and appeared to be caused, at least in part, by a marked increase in hepatic tumor necrosis factor-α and interleukin-6 mRNA expression accompanied by elevated levels of inhibitors of GH signaling, namely cytokine-inducible suppressors of cytokine signaling-1 and -3 and cytokine-inducible SH2 protein (CIS). Nuclear phosphorylated STAT5b levels were significantly depressed to 61% of the control values and represent a potential cause of the reduced GH-induced IGF-I expression. In addition, binding of phosphorylated STAT5b to DNA was reduced to an even greater extent and averaged 17% of the normal control value. This provides a further explanation for the impaired IGF-I gene transcription. Interestingly, when endotoxin-treated rats were treated with GH, there was a marked increase in proinflammatory cytokine gene expression in the liver. If such a response were to occur in humans, this might provide a partial explanation for the adverse effect of GH treatment reported in critically ill patients.

Insulin-like growth factor-I restores the reduced somatostatinergic tone controlling growth hormone secretion in cirrhotic rats

2001 ◽  
Vol 21 (6) ◽  
pp. 405-409 ◽  
Author(s):  
Inma Castilla-Cortázar ◽  
M. Aurelia Aliaga-Montilla ◽  
Javier Salvador ◽  
María García ◽  
Gloria Delgado ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

Effects of environmental salinity on somatic growth and growth hormone/insulin-like growth factor-I axis in juvenile tilapia Oreochromis mossambicus

2007 ◽  
Vol 73 (5) ◽  
pp. 1025-1034 ◽  
Author(s):  
Sameh MAGDELDIN ◽  
Katsuhisa UCHIDA ◽  
Tetsuya HIRANO ◽  
E Gordon GRAU ◽  
Ahmed ABDELFATTAH ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Somatic Growth ◽  
Oreochromis Mossambicus ◽  
Insulin Like Growth Factor ◽  
Environmental Salinity ◽  
Factor I ◽  
Growth Factor I

Impaired growth in Rabson-Mendenhall syndrome: lack of effect of growth hormone and insulin-like growth factor-I.

1994 ◽  
Vol 79 (3) ◽  
pp. 799-805
Author(s):  
N Longo ◽  
R Singh ◽  
L D Griffin ◽  
S D Langley ◽  
J S Parks ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I
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