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      Liver-derived insulin-like growth factor I (IGF-I) is the principal source of IGF-I in blood but is not required for postnatal body growth in mice.

      Proceedings of the National Academy of Sciences of the United States of America
      Aging, metabolism, Animals, Body Weight, Insulin-Like Growth Factor I, biosynthesis, deficiency, genetics, Liver, Mice, Mice, Knockout

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          Abstract

          The body growth of animals is regulated by growth hormone and IGF-I. The classical theory of this regulation is that most IGF-I in the blood originates in the liver and that body growth is controlled by the concentration of IGF-I in the blood. We have abolished IGF-I production in the livers of mice by using the Cre/loxP recombination system. These mice demonstrated complete inactivation of the IGF-I gene in the hepatocytes. Although the liver accounts for less than 5% of body mass, the concentration of IGF-I in the serum was reduced by 75%. This finding confirms that the liver is the principal source of IGF-I in the blood. However, the reduction in serum IGF-I concentration had no discernible effect on postnatal body growth. We conclude that postnatal body growth is preserved despite complete absence of IGF-I production by the hepatocytes.

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          Author and article information

          Journal
          10359843
          22065
          10.1073/pnas.96.12.7088

          Chemistry
          Aging,metabolism,Animals,Body Weight,Insulin-Like Growth Factor I,biosynthesis,deficiency,genetics,Liver,Mice,Mice, Knockout

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