Sjögren K, Liu J L, Blad K, Skrtic S, Vidal O, Wallenius V, LeRoith D, Törnell J, Isaksson O G, Jansson J O, Ohlsson C
Department of Internal Medicine, Division of Endocrinology, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden.
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):7088-92. doi: 10.1073/pnas.96.12.7088.
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.
动物的身体生长受生长激素和胰岛素样生长因子-I（IGF-I）调节。这种调节的经典理论是，血液中的大多数IGF-I起源于肝脏，且身体生长由血液中IGF-I的浓度控制。我们通过使用Cre/loxP重组系统消除了小鼠肝脏中的IGF-I产生。这些小鼠的肝细胞中IGF-I基因完全失活。尽管肝脏占体重不到5%，但血清中IGF-I的浓度降低了75%。这一发现证实肝脏是血液中IGF-I的主要来源。然而，血清IGF-I浓度的降低对出生后身体生长没有明显影响。我们得出结论，尽管肝细胞完全不产生IGF-I，但出生后身体生长仍得以维持。
