The aim of this study was to investigate the relationship between IGF-1 standard deviation score (IGF-1 SDS) and LDL-C level in children and adolescents with short stature.
Detection of GH and IGFBP-3 are important for the early diagnosis and comprehensive evaluation of children with dwarfism, and also in the detection of IGF-1 can reflect the therapeutic effect of dwarfism on recombinant human growth hormone (rhGH) treatment, which is worthy of application in clinics.
Since GH and IGF-I act on all these systems, we decided to study those parameters in a cohort of individuals with severe short stature due to untreated isolated GH deficiency (IGHD) caused by a mutation in the GHRH receptor gene.
However, other as yet unknown mechanisms not associated with the growth hormone (GH)-IGF-1 axis could be involved in growth retardation in idiopathic short stature.
Growth hormone and Insulin-like growth factor-I (IGF-I) modulate the expression of L-type amino acid transporters in the muscles of spontaneous dwarf rats and L6 and C2C12 myocytes.
While genetic causes of short stature were previously thought to primarily be associated with the GH-IGF-I axis, it is now established that multiple genetic anomalies not associated with the GH-IGF-I axis can result in short stature.
In this context, and when studying the GH/IGF-I axis of subjects with two different syndromes that include severe short stature (SSS), we noticed different metabolic phenotypes in each cohort.
Linear growth restriction is a unique feature of paediatric inflammatory bowel diseases (IBD), and reduced insulin-like growth factor (IGF-1) is a major determinant of short stature.
The insulin-like growth factor1 receptor (IGF1R) is important in growth and development, and inactivating <i>IGF1R</i> mutations cause short stature and relatively high levels of serum IGF-I.
Measurement of serum IGF-I and IGF-binding protein (IGFBP)-3 concentrations can complement assessment of GH status in the investigation of short stature and contribute to prediction of growth response during GH therapy.
Letter to the Editor: History and clinical implications of PAPP-A2 in human growth: When reflecting on idiopathic short stature leads to a specific and new diagnosis: Understanding the concept of "low IGF-I availability".
A molecular diagnosis for short stature is important for affected individuals and their families and might inform treatment decisions surrounding use of growth hormone or insulin-like growth factor 1 therapy.
Baseline Insulin like growth factor binding protein 3 (IGFBP - 3) along with ∆ IGF - 1 in the first 3 months of GH therapy level can be a marker of growth response to the rGH and/or rIGF - 1 therapy in children with non - growth hormone deficiency short stature.
Although metabolic outcomes may be aided by dual therapy with GI and IGF-I, the one published study of the combination approach to treat children with non-GH-deficient short stature showed only a meager additional height response compared to that achieved with GH alone.
Ames dwarf mice are deficient in GH, prolactin, and thyrotropin, whereas GHRKOs are GH resistant and are dwarf with decreased circulating IGF-1 and increased GH.
Fibroblasts of GH/IGF-1-deficient Snell dwarf mice also exhibited improved DNA repair capacity, showing that the persisting influence of peripubertal GH/IGF-1 status is not species-dependent.
We undertook a prospective study of 132 patients with short stature and suspected GH or IGF-1 insensitivity referred to our centre for genetic analysis.