<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>We investigated the changes in GH-IGF-I axis in
non-obese diabetic (NOD)-mice, a model of insulin dependent
diabetes mellitus. Diabetic female NOD
mice and their age- and sex-matched controls were
sacrificed at 4, 14, 21 and 30 days (<italic>30d DM</italic>) after the
onset of glycosuria. Serum GH levels increased and
serum IGF-I levels decreased in the 30d DM group
(182 ± 32% and 45 ± 24% of age-matched controls
respectively, <italic>p</italic> &lt; 0.05). Another group (<italic>30d DM + I</italic>)
was given SC insulin, and its serum IGF-I levels
remained decreased. Liver GH receptor (GHR) and
GH binding protein (GHBP) mRNA levels, as well
as liver membrane GH binding assays were deeply
decreased in the 30d DM group in comparison to
controls. GHR message and binding capacity remained
decreased in the 30d DM + I group. Renal
GHR mRNA was decreased at 21d DM but not at
14d DM, whereas GHBP mRNA remained unchanged
throughout the experiment. In conclusion,
increased serum GH levels are documented in NOD
diabetic mice, similarly to the changes described in
humans. The decrease in GHR levels and decreased
serum IGF-I in spite of increased circulating GH
suggest a state of GH resistance.</p>
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Int J Exp Diabetes Res. 2000; 1(1):9-18