Klara Sjögren1, Jun‐Li Liu1, K. Blad1, Stanko Skrtic1, Olle Vidal1, Ville Wallenius1, Derek LeRoith1, Jan Törnell1, Olle Isaksson1, John‐Olov Jansson1, Claes Ohlsson1
1Department of Internal Medicine, Division of Endocrinology, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden; Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10 Room 8S235A, 10 Center Drive, MCS-1770, Bethesda, MD 20892-1770; and Department of Physiology, University of Göteborg, S-405 30 Göteborg, Sweden
Tóm tắt
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.
