Summary
The pygmy mouse has been proposed as a model for growth hormone resistance; it has
normal serum somatomedin levels and does not respond to growth hormone treatment.
In order to determine if the growth impairment is caused by a defect in somatomedin
binding or in postreceptor action of somatomedin we compared fibroblasts derived from
pygmy mice with those from normal appearing littermates. Using multiplication-stimulating
activity (MSA) as a model somatomedin we found a normal Ka of binding to the cell surface MSA receptor but a significantly increased number
of MSA receptors on the fibroblasts derived from pygmy mice. Studies of thymidine
incorporation into DNA failed to demonstrate a difference between pygmy and normal
fibroblasts in their responses to MSA alone, but there was a significantly greater
thymidine incorporation into the DNA of normal fibroblasts when both competence factor
(plateletderived growth factor) and progression factors (somatomedins and growth hormone
deficient platelet-poor plasma) were present in the test medium. On the other hand,
cell proliferation studies did not demonstrate a consistent difference in the growth
rate of normal versus pygmy fibroblasts. The data support the conclusion that the
impaired growth of the pygmy mouse in vivo may be caused by factors which lie outside
of the growth hormone-somato-medin pathway.
Key-Words:
Pygmy Mice
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Multiplication-Stimulating Activity
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Somatomedins
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Somatomedin Receptors
