The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Metabolic Actions of Insulin-Like Growth Factor-I in Normal Physiology and Diabetes
Open accessAbstract
Synopsis Insulin-like growth factor-I (IGF-I) is closely related to insulin but has distinct metabolic actions. IGF-I is an important stimulant of protein synthesis in muscle but it also stimulates free fatty acid utilization. Important indirect effects of IGF-I that influence metabolism include suppression of growth hormone secretion and at supraphysiologic concentrations suppression of insulin secretion. IGF-I actions are regulated by IGF binding proteins and in obesity and metabolic syndrome there is major dysregulation of IGF binding protein secretion resulting in alterations in the concentration of free IGF-I and IGF-I actions. In type 1 diabetes, IGF-I synthesis is markedly impaired and in type 2 diabetes multiple changes occur in IGF-I actions including sensitization to its mitogenic actions in some target tissues. Administration of IGF-I to patients with extreme insulin resistance results in improvement in glycemic control and IGF-I has been shown to be associated with lowering glucose and enhancing insulin sensitivity in both type 1 and type 2 diabetes. However diabetics are also quite sensitive to stimulation of side effects in response to IGF-I and this has greatly limited its usefulness as a hypoglycemic agent. IGF-I coordinately links growth hormone and insulin actions as well as having direct effects on intermediary metabolism.
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Cites
Skeletal muscle hypertrophy and atrophy signaling pathways
Glass, D. J. (2005) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2005.04.018 · Cited by 1,106 · cited 1×
“Conversely mice that have been genetically altered to constitutively activate this complex are resistant to the anticatabolic effects of IGF-I (17).”
Sandhu, M. S., Heald, A. H., Gibson, J. M., Cruickshank, J. K., Dunger, D. B., & Wareham, N. J. (2002) · The Lancet · doi:10.1016/s0140-6736(02)08655-5 · Cited by 470
Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes
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Self-citationO’Connor, J. C., McCusker, R. H., Strle, K., Johnson, R. W., Dantzer, R., & Kelley, K. W. (2008) · Cellular Immunology · doi:10.1016/j.cellimm.2007.09.010 · Cited by 238
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Mitochondrial quality control and muscle mass maintenance.
Romanello, V., & Sandri, M. (2016) · Frontiers in Physiology · doi:10.3389/fphys.2015.00422 · Cited by 434
Insulin-Like Growth Factor 1 (IGF-1) Signaling in Glucose Metabolism in Colorectal Cancer
Kasprzak, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126434 · Cited by 248
ATP Citrate Lyase Improves Mitochondrial Function in Skeletal Muscle
Das, S., Morvan, F., Jourde, B., Meier, V., Kahle, P., Brebbia, P., Toussaint, G., Glass, D. J., & Fornaro, M. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.05.006 · Cited by 91
Vitale, G., Brugts, M. P., Ogliari, G., Castaldi, D., Fatti, L. M., Varewijck, A. J., Lamberts, S. W., Monti, D., Bucci, L., Cevenini, E., et al. (2012) · Aging · doi:10.18632/aging.100484 · Cited by 90
Sarcopenic obesity: Myokines as potential diagnostic biomarkers and therapeutic targets?
Guo, A., Li, K., & Xiao, Q. (2020) · Experimental Gerontology · doi:10.1016/j.exger.2020.111022 · Cited by 83
Metadata
- Authors
- Clemmons, D. R.
- Venue
- Endocrinology and Metabolism Clinics of North America
- Publisher
- Elsevier BV
- Published
- 2012-06
- Volume
- 41
- Issue
- 2
- Pages
- 425-443
- ISSN
- 0889-8529 (ISSN-L)
- OpenAlex
- W2070089423
- Cited by
- 297
- References
- 6
- FWCI
- 12.66
- Type
- journal article
- Language
- en
- Open access
- green
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