Journal
DEVELOPMENTAL BIOLOGY
Volume 229, Issue 1, Pages 141-162Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/dbio.2000.9975
Keywords
growth; growth rate; growth retardation; growth hormone; growth hormone receptor; insulin-like growth factor 1; ossification; chondrocyte
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Funding
- NICHD NIH HHS [HD34526] Funding Source: Medline
- NIMH NIH HHS [MH50733] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD034526] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH050733] Funding Source: NIH RePORTER
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To examine the relationship between growth hormone (GH) and insulin-like growth factor 1 (IGF1) in controlling postnatal growth, we performed a comparative analysis of dwarfing phenotypes manifested in mouse mutants lacking GH receptor, IGF1, or both. This genetic study has provided conclusive evidence demonstrating that GH and IGF1 promote postnatal growth by both independent and common functions, as the growth retardation of double Ghr/Igf1 nullizygotes is more severe than that observed with either class of single mutant. In fact, the body weight of these double-mutant mice is only similar to 17% of normal and, in absolute magnitude (similar to5 g), only twice that of the smallest known mammal. Thus, the growth control pathway in which the components of the GH/IGF1 signaling systems participate constitutes the major determinant of body size. To complement this conclusion mainly based on extensive growth curve analyses, we also present details concerning the involvement of the GH/IGF1 axis in linear growth derived by a developmental study of long bone ossification in the mutants. (C) 2001 Academic Press.
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