The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Insulin-like growth factor 1 (IGF-1): a growth hormone
Open accessAbstract
AIM: To contribute to the debate about whether growth hormone (GH) and insulin-like growth factor 1 (IGF-1) act independently on the growth process. METHODS: To describe growth in human and animal models of isolated IGF-1 deficiency (IGHD), such as in Laron syndrome (LS; primary IGF-1 deficiency and GH resistance) and IGF-1 gene or GH receptor gene knockout (KO) mice. RESULTS: Since the description of LS in 1966, 51 patients were followed, many since infancy. Newborns with LS are shorter (42-47 cm) than healthy babies (49-52 cm), suggesting that IGF-1 has some influence on intrauterine growth. Newborn mice with IGF-1 gene KO are 30% smaller. The postnatal growth rate of patients with LS is very slow, the distance from the lowest normal centile increasing progressively. If untreated, the final height is 100-136 cm for female and 109-138 cm for male patients. They have acromicia, organomicria including the brain, heart, gonads, genitalia, and retardation of skeletal maturation. The availability of biosynthetic IGF-1 since 1988 has enabled it to be administered to children with LS. It accelerated linear growth rates to 8-9 cm in the first year of treatment, compared with 10-12 cm/year during GH treatment of IGHD. The growth rate in following years was 5-6.5 cm/year. CONCLUSION: IGF-1 is an important growth hormone, mediating the protein anabolic and linear growth promoting effect of pituitary GH. It has a GH independent growth stimulating effect, which with respect to cartilage cells is possibly optimised by the synergistic action with GH.
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Dehkhoda, F., Lee, C. M. M., Medina, J., & Brooks, A. J. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00035 · Cited by 304
Implications of Insulin-Like Growth Factor-1 in Skeletal Muscle and Various Diseases
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Self-citationProtective role of IGF-1 and GLP-1 signaling activation in neurological dysfunctions
Bhalla, S., Mehan, S., Khan, A., & Rehman, M. U. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104896 · Cited by 108
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Metadata
- Authors
- Laron, Z.
- Venue
- Molecular Pathology
- Publisher
- BMJ
- Published
- 2001-10
- Volume
- 54
- Issue
- 5
- Pages
- 311-316
- ISSN
- 1366-8714 (ISSN-L)
- 1472-4154
- OpenAlex
- W1989308141
- Cited by
- 608
- References
- 63
- FWCI
- 2.70
- Type
- journal article
- Language
- en
- Open access
- bronze
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