The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
Mechanisms of Disease: metabolic effects of growth hormone and insulin-like growth factor 1
Abstract
Insulin-like growth factor (IGF) 1 is a member of a family that is involved in growth, development, cell differentiation, and metabolism. IGF1, IGF2 and insulin act primarily through tyrosine-kinase-linked receptors--the IGF1 receptor (IGF1R) and insulin receptor (IR). The IGF1R binds IGF1 and IGF2 with high affinity and the IR binds insulin with high affinity; however, since both receptors share a high degree of structural and functional homology, the IGF1R can bind insulin and the IR can bind the IGFs with reduced affinity. These two receptors can, moreover, form heterodimers, which bind both ligands. Upon binding to the receptors, cascades of tyrosine and serine kinases are stimulated to facilitate growth or metabolism. The IGF2 receptor is a scavenger receptor, and is, therefore, not involved in mediation of growth or metabolic effects of the IGF family and will not be discussed in the current article. IGF1 is a major gene target of growth hormone and its product mediates many of the actions of growth hormone on growth and development; however, IGF1 has actions distinct from those of growth hormone in carbohydrate, lipid, and protein metabolism. For example, excess growth hormone causes insulin resistance and hyperglycemia, whereas IGF1 has insulin-like effects that reduce blood glucose levels and has been used experimentally to treat both type 1 and type 2 diabetes.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“The effects of growth hormones on glucose regulation is intricate and changes substantially with different dosage and treatment duration (49, 51).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [49]
In the citing paper
“on glucose regulation is intricate and changes substantially with different dosage and treatment duration (49, 51).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [49]
In the citing paper
“The effects of growth hormones on glucose regulation is intricate and changes substantially with different dosage and treatment duration (49, 51).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [49]
In the citing paper
“Thus, growth hormone in contrast to IGF-1 has many catabolic effects leading to provision of energy-rich substrates to an activated immune system in inflammation.”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [57]
Citations
Cites
Cellular Actions of the Insulin-Like Growth Factor Binding Proteins
Firth, S. M., & Baxter, R. C. (2002) · Endocrine Reviews · doi:10.1210/er.2001-0033 · Cited by 1,739
Effects of Human Growth Hormone in Men over 60 Years Old
Rudman, D. R., Feller, A. G., Nagraj, H. S., Gergans, G. A., Lalitha, P. Y., Goldberg, A. F., Schlenker, R. A., Cohn, L., Rudman, I. W., & Mattson, D. E. (1990) · New England Journal of Medicine · doi:10.1056/nejm199007053230101 · Cited by 1,545
Normal growth and development in the absence of hepatic insulin-like growth factor I
Yakar, S., Liu, J., STANNARD, B. S., Butler, A. A., Accili, D., Sauer, B., & LeRoith, D. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.13.7324 · Cited by 1,418
Self-citationIncreased mortality associated with growth hormone treatment in critically ill adults
Takala, J., Ruokonen, E., Webster, N. R., Nielsen, M. S., Zandstra, D. F., Vundelinckx, G., & Hinds, C. J. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909093411102 · Cited by 1,023
INCREASED MORTALITY ASSOCIATED WITH GROWTH HORMONE TREATMENT IN CRITICALLY ILL ADULTS
Akala, J. U. T., Uokonen, E. S. R., Igel, N., Ebster, R. W., Ielsen, M. I. S. N., Andstra, D. U. F. Z., Undelinckx, G. U. V., & Inds, H. J. H. (1999) · Cited by 889
Treatment of adults with growth hormone (GH) deficiency with recombinant human GH.
Bengtsson, B. Å., Edén, S., Lönn, L., Kvist, H., Stokland, A. M., Lindstedt, G., Bosaeus, I. G., Tölli, J., Sjöström, L., & Isaksson, O. G. P. (1993) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.76.2.8432773 · Cited by 780
Roles of Growth Hormone and Insulin-like Growth Factor 1 in Mouse Postnatal Growth
Lupu, F. I., Terwilliger, J. D., Lee, K., Segre, G. V., & Efstratiadis, A. (2001) · Developmental Biology · doi:10.1006/dbio.2000.9975 · Cited by 769
Fat cell adrenergic receptors and the control of white and brown fat cell function
Lafontan, M., & Berlan, M. (1993) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)37695-1 · Cited by 644
Assessment of Growth Parameters and Life Span of GHR/BP Gene-Disrupted Mice 1
Coschigano, K. T., Clemmons, D., Bellush, L. L., & Kopchick, J. J. (2000) · Endocrinology · doi:10.1210/endo.141.7.7586 · Cited by 611
Targeted Disruption of the β3-Adrenergic Receptor Gene
Susulic, V. S., Frederich, R. C., Lawitts, J. A., Tozzo, E., Kahn, B. B., Harper, M., Himms‐Hagen, J., Flier, J. S., & Lowell, B. B. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.49.29483 · Cited by 493
Cited by
Sorted by citations
Vigneri, P., Frasca, F., Sciacca, L., Pandini, G., & Vigneri, R. (2009) · Endocrine Related Cancer · doi:10.1677/erc-09-0087 · Cited by 1,009
Acromegaly pathogenesis and treatment
Melmed, S. K. (2009) · Journal of Clinical Investigation · doi:10.1172/jci39375 · Cited by 704
Kumar, K. G., Trevaskis, J. L., Lam, D. D., Sutton, G. M., Koza, R. A., Chouljenko, V. N., Kousoulas, K. G., Rogers, P. M., Kesterson, R. A., Thearle, M. S., et al. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.10.011 · Cited by 516
Inhibition of Growth Hormone Signaling by the Fasting-Induced Hormone FGF21
Inagaki, T., Lin, V. Y., Goetz, R., Mohammadi, M., Mangelsdorf, D. J., & Kliewer, S. A. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2008.05.006 · Cited by 409
Clemmons, D. R. (2011) · Clinical Chemistry · doi:10.1373/clinchem.2010.150631 · Cited by 352
Metadata
- Authors
- LeRoith, D., & Yakar, S.
- Affiliations
- Mount Sinai Hospital (US)
- Corresponding author
- LeRoith, Derek
- ORCID
- Yakar, Shoshana
- Venue
- Nature Clinical Practice Endocrinology & Metabolism
- Published
- 2007-03
- Volume
- 3
- Issue
- 3
- Pages
- 302-310
- ISSN
- 1745-8366 (ISSN-L)
- 1745-8374
- OpenAlex
- W2084967524
- Cited by
- 344
- References
- 71
- Citations by year
- 2026: 11 · 2025: 22 · 2024: 21 · 2023: 18 · 2022: 20 · 2021: 17 · 2020: 25 · 2019: 20 · 2018: 21 · 2017: 14 · 2016: 19 · 2015: 17 · 2014: 22 · 2013: 15 · 2012: 24
- FWCI
- 1.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Clinical Practice Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Keywords
- insulin-like growth factor I, growth hormone, IGF-1 receptor, insulin receptor, receptor heterodimerization, tyrosine kinase signaling, insulin-like growth factor II, insulin resistance, hyperglycemia, glucose metabolism, lipid metabolism, protein metabolism, diabetes treatment
- MeSH terms
- Animals, Humans, Insulin-Like Growth Factor I, Models, Biological, Growth Hormone, Models, Animal, Growth and Development, Metabolic Networks and Pathways
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
