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Unbound (bioavailable) IGF1 enhances somatic growth
Sebastien Elis1, Yingjie Wu, Hayden-William Courtland
1Division of Endocrinology, Diabetes and Bone Disease, Mount Sinai School of Medicine, New York, NY 10029, USA.
Disease Models & Mechanisms
|June 2, 2011
Summary
Insulin-like growth factor-1 (IGF1) binding to IGF-binding proteins (IGFBPs) is crucial for normal growth. Disrupting this binding leads to altered growth patterns and organ development in mice.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- Insulin-like growth factor-1 (IGF1) is vital for growth, cellular transformation, regeneration, immunity, musculoskeletal development, and aging.
- IGF1 bioactivity is regulated by binding to IGF-binding proteins (IGFBPs) and the acid-labile subunit (ALS).
Purpose of the Study:
- To investigate if IGF1 binding to IGFBPs is essential for normal growth and development.
- To generate and analyze mouse models with mutated IGF1 exhibiting reduced IGFBP affinity.
Main Methods:
- Gene targeting to create knock-in mouse models (KID and KIR) with mutated IGF1 (Des-Igf1 and R3-Igf1).
- Analysis of serum IGF1 levels, growth hormone, and IGF1-IGFBP-ALS ternary complex formation.
- Assessment of body weight, length, lean mass, organ size, mammary gland complexity, and skeletal acquisition.
Main Results:
- Mutant mice (KID and KIR) showed reduced serum IGF1 and increased growth hormone levels.
- Ternary complex formation was significantly reduced in mutant mice compared to wild type.
- Mutant mice exhibited increased body weight, lengths, lean mass, organomegaly (spleen, kidneys, uterus), enhanced mammary gland complexity, and skeletal acquisition.
Conclusions:
- IGF1 complex formation with IGFBPs is fundamental for establishing normal body and organ size.
- Uncontrolled IGF bioactivity, due to reduced IGFBP binding, can lead to pathological conditions.
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