Effects of Vitamin A Deficiency and Retinoic Acid Treatment on Expression of a Phosphoenolpyruvate Carboxykinase-Bovine Growth Hormone Gene in Transgenic Mice

1995 ◽  
Vol 213 (2) ◽  
pp. 706-714 ◽  
Author(s):  
D.J. Shin ◽  
A.Y. Tao ◽  
M.M. Mcgrane
Keyword(s):  
Growth Hormone ◽  
Retinoic Acid ◽  
Vitamin A ◽  
Transgenic Mice ◽  
Acid Treatment ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Vitamin A Deficiency ◽  
Bovine Growth Hormone ◽  
Growth Hormone Gene ◽  
Retinoic Acid Treatment

Effects of bovine growth hormone (GH) expression in transgenic mice on serum and pituitary immunoreactive mouse GH levels and pituitary GH-releasing factor binding sites

1993 ◽  
Vol 129 (5) ◽  
pp. 446-452 ◽  
Author(s):  
AI Sotelo ◽  
A Bartke ◽  
D Turyn
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Binding Sites ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Serum Levels ◽  
Bovine Growth Hormone ◽  
Complete Suppression ◽  
Over Expression ◽  
Pituitary Glands ◽  
Scatchard Plots

Pituitary and serum levels of homologous growth hormone (GH) and characteristics of specific GH-releasing factor (GHRF) binding to pituitary homogenates were examined in transgenic mice expressing bovine GH (bGH) gene regulated by different promoters [mouse metallothionein-I (MT) or phosphoenolpyruvate carboxykinase (PEPCK)] and in their normal littermates. Pituitary GH concentration and GHRF binding were reduced by approximately 50% in transgenic MT-bGH mice in which serum bGH levels were about 20 μg/l and by approximately 95% in transgenic PEPCK-bGH mice in which serum bGH levels were tenfold higher. Suppression of plasma immunoreactive mouse GH (mGH) levels was detected in MT-bGH but not in PEPCK-bGH animals, presumably due to cross-reaction of the antiserum employed with bGH. Scatchard plots of GHRF binding to washed homogenates of pituitary glands from normal and young adult MT-bGH transgenic mice were curvilinear, indicating the presence of two types of binding sites, with low and high affinities. Both types of binding sites were reduced in number in MT-bGH transgenic mice without changes in their affinity. In 5–7-month-old MT-bGH transgenic mice there were changes in pituitary GH levels, in GHRF binding levels and in characteristics of GHRF binding that closely resembled the alterations described previously in aging rats. We conclude that over-expression of heterologous GH genes in transgenic mice can lead to partial or virtually complete suppression of somatotroph function, depending on the levels of heterologous GH in the circulation, and that transgenic MT-bGH mice exhibit symptoms of remarkably early onset of neuroendocrine aging.

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