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Submitted on July 21, 2003
Accepted on September 25, 2003
1 Institute for Endocrinology and Diabetes, National Center for Childhood Diabetes, Schneider Children's Medical Center of Israel and Felsenstein Medical Research Center, Petah Tikva and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Anatomy and Cell Biology, The Rappaport Faculty of Medicine, Technion, Israel. Laboratory of Molecular Endocrinology, Ben Gurion University of the Negev, Beer Sheva, Israel.
* To whom correspondence should be addressed. E-mail: mosheph{at}post.tau.ac.il.
Caloric imbalance, particularly in critical periods of growth and development, is often the underlying cause of growth abnormalities. Serum levels of leptin are elevated in obesity and low in malnutrition and malabsorption. The aim of the present study was to determine if leptin integrates energy levels and growth in vivo, as shown previously in our ex vivo experiments, even in the presence of caloric restriction. In the first part of the study, mice were divided into 3 groups. Two groups were fed ad libitum and received leptin or vehicle only and the third group was pair fed to the group injected with leptin, to dissociate leptin's effect on growth from its effect on food consumption. Mice given leptin had a significantly greater tibial length than untreated pair fed animals, and a similar tibial length to control mice fed ad libitum despite their lower weight. In addition, leptin significantly increased the overall size of the epiphyseal growth plate by 11%. On immuno-histochemistry and in situ hybridization studies leptin stimulated both the proliferation and differentiation of the tibial growth plate chondrocytes, without affecting the overall organization of the plate. There was also a marked increase in the expression and the level of IGF-IR. In the second part of the study, 2 groups of mice were fed only 60% of their normal chow, one was injected with leptin and the other with vehicle alone. Caloric deprivation by itself reduced serum levels of IGF-I by 70%, and the length of the tibia by 5%. Leptin treatment corrected the fasting-induced growth deficiency, but further reduced the level of serum IGF-I.
These results indicate that leptin stimulate growth even in the presence of caloric restriction independently of peripheral IGF-I.
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