The somatomedin hypothesis revisited in a transgenic model.
Studies of insulin-like growth factor I (IGF-I) gene knockout mice models have clearly shown that IGF-I is necessary for prenatal as well as postnatal body growth in mice. Clinical studies of a patient with an IGF-I gene defect which caused complete absence of IGF-I, verified that it is important for intrauterine and postnatal growth. Recent studies of mice with liver-specific and inducible IGF-I gene knockout indicated that liver-derived IGF-I is not necessary for postnatal body growth, although serum IGF-I levels are decreased by more than 80% in these mice. Therefore, extrahepatic IGF-I is sufficient for maintenance of postnatal body growth in mice. Further investigations are needed to assess whether liver-derived circulating IGF-I is essential for other biological functions.
Isaksson
O
O
Research Center for Endocrinology and Metabolism, Sahlgrenska University Hospital, Göteborg, Sweden.
Ohlsson
C
C
Sjögren
K
K
Wallenius
K
K
Jansson
J O
JO
D000818:Animals; D001835:Body Weight / Q000235:genetics*; D005818:Genetic Engineering / Q000379:methods; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D019426:Integrases / Q000235:genetics; D008099:Liver / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009929:Organ Size; D013002:Somatomedins / Q000502:physiology*; D014764:Viral Proteins / Q000235:genetics
D013002:Somatomedins; D014764:Viral Proteins; D007334:Insulin-Like Growth Factor I; C045073:Cre recombinase; D019426:Integrases