Insulin Signaling Through the Insulin Receptor Increases Linear Growth Through Effects on Bone and the Growth Hormone (GH)–IGF-1 Axis
An erratum to this article was published (J Clin Endocrinol Metab, 17 Jun 2025 ↗)
Authors' conclusion
Patients with hyperinsulinemia and impaired InsR function exhibit impaired growth and lower BMD, whereas elevated InsR signaling (CGL) causes accelerated growth and higher BMD. These patients demonstrate that insulin action through the InsR stimulates direct anabolic effects in bone and indirect actions through the growth hormone (GH)-IGF-1 axis. TBIR patients exhibit abnormalities in the GH axis that resolve when InsR signaling is restored, supporting a causal relationship between InsR and GH axis signaling.
Study context
- Population
- Rare disease patients with hyperinsulinemia and impaired insulin receptor (InsR) function (INSR variants, TBIR) or with CGL, National Institutes of Health
- Participants
- 23 / 13 / 17 / 8
- Exposure
- INSR-/- vs CGL
- CGLn = 23reference
- INSR-/-n = 13
- INSR+/-n = 17
- TBIRn = 8
- Outcome
- Main outcome measures: SD scores (SDS) for height, BMI, IGF-1 and bone mineral density (BMD); IGFBP-1 and IGFBP-3
Methodological detailssingle-centre, Conducted at the National Institutes of Health
- Single-centre
- Conducted at the National Institutes of Health
Main finding
As reported in the abstract
- INSR+/- were variable
- INSR-/- vs CGL: P < 0.05 for all
Observational data: associations, not effects.
Further findings
- Remission of TBIR lowered insulin and IGFBP-1, and increased IGF-1 and IGFBP-3 (P < .05)
Original publication
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