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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.
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“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]
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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
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