Effect of Nutrition on Statural Growth

Gat-Yablonski, Galia; Luca, Francesco De

doi:10.1159/000456547

Cited by 30 publications

(20 citation statements)

References 172 publications

(229 reference statements)

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“…Elevated circulating IGF-I levels were absent prior to rGH therapy for 23.8% of the patients in our cohort but IGF-I levels rose markedly after initiating rGH treatment. The absence of high IGF-I levels prior to rGH therapy can be explained by the previously described feeding difficulties of some patients with IGF1R defects, which can lead to nutritional deficiency and low basal levels of IGF-I 31. This pattern of low IGF-I levels which increase rapidly after initiating rGH therapy, should alert clinicians to the possibility of an IGF1R defect in a child born SGA, especially with the presence of microcephaly.…”

Section: Discussionmentioning

confidence: 97%

Increasing knowledge in IGF1R defects: lessons from 35 new patients

et al. 2019

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BackgroundThe type 1 insulin-like growth factor receptor (IGF1R) is a keystone of fetal growth regulation by mediating the effects of IGF-I and IGF-II. Recently, a cohort of patients carrying an IGF1R defect was described, from which a clinical score was established for diagnosis. We assessed this score in a large cohort of patients with identified IGF1R defects, as no external validation was available. Furthermore, we aimed to develop a functional test to allow the classification of variants of unknown significance (VUS) in vitro.MethodsDNA was tested for either deletions or single nucleotide variant (SNV) and the phosphorylation of downstream pathways studied after stimulation with IGF-I by western blot analysis of fibroblast of nine patients.ResultsWe detected 21 IGF1R defects in 35 patients, including 8 deletions and 10 heterozygous, 1 homozygous and 1 compound-heterozygous SNVs. The main clinical characteristics of these patients were being born small for gestational age (90.9%), short stature (88.2%) and microcephaly (74.1%). Feeding difficulties and varying degrees of developmental delay were highly prevalent (54.5%). There were no differences in phenotypes between patients with deletions and SNVs of IGF1R. Functional studies showed that the SNVs tested were associated with decreased AKT phosphorylation.ConclusionWe report eight new pathogenic variants of IGF1R and an original case with a homozygous SNV. We found the recently proposed clinical score to be accurate for the diagnosis of IGF1R defects with a sensitivity of 95.2%. We developed an efficient functional test to assess the pathogenicity of SNVs, which is useful, especially for VUS.

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Section: Discussionmentioning

confidence: 97%

Increasing knowledge in IGF1R defects: lessons from 35 new patients

et al. 2019

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“…IGF-1 is also an important growth hormone, mediating protein anabolism and linear growth [ 27 ]. IGF-1 serum levels are responsive to improved nutritional status [ 61 ] and high-protein intake [ 48 , 62 ]. Protein restriction in children results in declined IGF-I concentrations [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Associations among High-Quality Protein and Energy Intake, Serum Transthyretin, Serum Amino Acids and Linear Growth of Children in Ethiopia

et al. 2018

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Limited evidence is available on the associations of high-quality protein and energy intake, serum transthyretin (TTR), serum amino acids and serum insulin-like growth factor-1 (IGF-1) with linear growth of young children. Data collected during the baseline of a randomized control trial involving rural Ethiopian children aged 6–35 months (n = 873) were analyzed to evaluate the associations among height/length-for-age z-scores, dietary intakes, and these biomarkers (i.e., serum level of TTR, IGF-1, tryptophan and lysine, and inflammation). The prevalence of stunting was higher for children >23 months (38%) than ≤23 months (25%). The prevalence of inflammation was 35% and of intestinal parasites 48%. Three-quarters of the children were energy deficient, and stunted children had lower daily energy intake that non-stunted children (p < 0.05). Intakes of tryptophan, protein, and energy, and serum levels of tryptophan and IGF-1 were positively correlated with the linear growth of children. Controlling for inflammation, intestinal parasites, and sociodemographic characteristics, daily tryptophan (b = 0.01, p = 0.001), protein (b = 0.01, p = 0.01) and energy (b = 0.0003, p = 0.04) intakes and serum TTR (b = 2.58, p = 0.04) and IGF-1 (b = 0.01, p = 0.003) were positively associated with linear growth of children. Linear growth failure in Ethiopian children is likely associated with low quality protein intake and inadequate energy intake. Nutrition programs that emphasize improved protein quantity and quality and energy intake may enhance the linear growth of young children and need to be further investigated in longitudinal and interventional studies.

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“…processes (Gat-Yablonski & De Luca 2017). To resume normal growth or initiate CUG, undernourished children must regain up to 85% of their weight for height (Kay's & Hindmarsh 2006).…”

Section: Introductionmentioning

confidence: 99%

Leptin stimulates aromatase in the growth plate: limiting catch-up growth efficiency

Masarwi

Shamir

Phillip

et al. 2018

Journal of Endocrinology

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Catch-up growth (CUG) in childhood is defined as periods of growth acceleration, after the resolution of growth attenuation causes, bringing the children back to their original growth trajectory. Sometimes, however, CUG is incomplete, leading to permanent growth deficit and short stature. The aim of this study was to investigate the mechanisms that limit nutritional-CUG. Specifically, we focused on the crosstalk between leptin, increased by re-feeding, and sex hormones, which increase with age. studies were performed in young male Sprague Dawley rats fed or subjected to 10/36 days of 40% food restriction followed by 90-120 days of re-feeding. studies were performed on ATDC5 cells. Analyses of mRNA and protein levels were done using qPCR and Western blot, respectively. CUG was complete in body weight and humerus length in animals that were food-restricted for 10 days but not for those food-restricted for 36 days. studies showed that leptin significantly increased aromatase gene expression and protein level as well as the expression of estrogen and leptin receptors in a dose- and time-dependent manner. The effect of leptin on aromatase was direct and was mediated through the MAPK/Erk, STAT3 and PI3K pathways. The crosstalk between leptin and aromatase in the growth plate suggests that re-feeding during puberty may lead to increased estrogen level and activity, and consequently, irreversible premature epiphyseal growth plate closure. These results may have important implications for the development of novel treatment strategies for short stature in children.

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Effect of Nutrition on Statural Growth

Cited by 30 publications

References 172 publications

Increasing knowledge in IGF1R defects: lessons from 35 new patients

Increasing knowledge in IGF1R defects: lessons from 35 new patients

Associations among High-Quality Protein and Energy Intake, Serum Transthyretin, Serum Amino Acids and Linear Growth of Children in Ethiopia

Leptin stimulates aromatase in the growth plate: limiting catch-up growth efficiency

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