Abstract
Insulin-like growth factor I (IGF-I) and insulin stem from a common precursor, are structural homologues, act through similar receptors and elicit insulin-like and growth-promoting effects in vitro and in vivo1,2. Serum IGF-I levels are controlled by growth hormone1, insulin3–6 and nutrition6–10. Insulin-deficient growth-arrested diabetic animals have reduced serum IGF-I levels which are restored towards normal by insulin but not by growth-hormone treatment3–6. Here we show that normal growth of diabetic rats is restored by infusion of recombinant human (rh)IGF-I without normalization of the blood sugar level and that insulin acts via an increase of IGF-I synthesis on growth of diabetic rats. We describe a new mechanism of endocrine control of growth in which IGF-I is the major stimulator at the cellular level. Growth hormone and insulin act mainly by modulating the hepatic synthesis of IGF-I.
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Scheiwiller, E., Guler, HP., Merryweather, J. et al. Growth restoration of insulin-deficient diabetic rats by recombinant human insulin-like growth factor I. Nature 323, 169–171 (1986). https://doi.org/10.1038/323169a0
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DOI: https://doi.org/10.1038/323169a0
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