Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID).
Our data showed that blood levels of growth hormone, which stimulates IGF-1 production in liver, were increased but could not overcome the IGF-1 deficiency.
These changes were not observed in iLID mice with a short-term (2 days) IGF-I depletion, despite a 70% reduction in their circulating IGF-I levels, indicating that a sustained IGF-I deficiency was necessary to alter the neutrophil phenotype.
Additionally, the impact of IGF-1 deficiency on a damaged liver was investigated in mice with a partial deficit of this hormone (Hz Igf1 <sup>+/-</sup>).
A partial IGF-1 deficiency murine model was used to investigate IGF-1's effects on liver by comparing wild-type controls, heterozygous igf1<sup>+/-</sup>, and heterozygous mice treated with IGF-1 for 10 days.
To determine the role of IGF-1 deficiency in the pathogenesis of CMHs, we induced hypertension in mice with liver-specific knockdown of IGF-1 (Igf1<sup>f/f</sup> + TBG-Cre-AAV8) and control mice by angiotensin II plus l-NAME treatment.
Age-related decline in circulating IGF-1 levels results in functional impairment of the cerebral microvessels; however, the mechanistic role of IGF-1 deficiency in impaired hippocampal microvascularization remains elusive.
The aim of this work was to confirm that heterozygous Igf-1 (+/-) mice (Hz) may be considered as an appropriate animal model to study conditions of IGF-1 deficiency, focusing on early ages.
Twenty-one children with severe IGFD were treated until adult or near-adult height under a predominantly open-label design.All patients were naive to IGF-I.
At the lower end of the GHRH-IGF-1 axis, primary IGF-1 deficiency and IGF-1 resistance due to defects within the IGF-1 and IGF-1 receptor (IGF-1R) genes account for approximately 10-15% of all cases with intrauterine and postnatal growth retardation.
Long-term auxological and pubertal outcome of patients with hereditary insulin-like growth factor-I deficiency (Laron and growth hormone-gene deletion syndrome) treated with recombinant human insulin-like growth factor-I.
To investigate whether congenital IGF1 deficiency confers protection against development of malignancies, by comparing the prevalence of malignancies in patients with congenital (secondary) deficiency of IGF1 with the prevalence of cancer in their family members.
Although IGFD can develop at any level of the GH-releasing hormone (GHRH)-GH-IGF axis, a differentiation should be made between GHD (absent to low GH in circulation) and IGFD (normal to high GH in circulation).
We assessed the efficacy and safety of recombinant human insulin-like growth factor 1 (IGF-1) therapy over a period of 7.5 years in a child with severe IGF-1 deficiency.
In our previous reports, liver- or pancreatic-specific IGF-I deficiency caused no decrease in β-cell mass; a general and β-cell-enriched IGF-I overexpression caused no change in normal islet cell growth.