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Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age
OBJECTIVE: Children born small for gestational age (SGA) are at risk for developing type 2 diabetes. Lipodystrophy leads to early type 2 diabetes and leptin reverses the metabolic consequences of the disease. Low IGF-binding protein 1 (IGFBP1) can predict the development of type 2 diabetes. The aim...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioScientifica
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680956/ https://www.ncbi.nlm.nih.gov/pubmed/23781317 http://dx.doi.org/10.1530/EC-12-0071 |
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author | Kistner, Anna Vanpée, Mireille Hall, Kerstin |
author_facet | Kistner, Anna Vanpée, Mireille Hall, Kerstin |
author_sort | Kistner, Anna |
collection | PubMed |
description | OBJECTIVE: Children born small for gestational age (SGA) are at risk for developing type 2 diabetes. Lipodystrophy leads to early type 2 diabetes and leptin reverses the metabolic consequences of the disease. Low IGF-binding protein 1 (IGFBP1) can predict the development of type 2 diabetes. The aim of this study was to determine leptin, insulin, and IGFBP1 in children and adult women born preterm or SGA to evaluate the role of leptin as a compensatory mechanism in insulin resistance development. METHODS: Seventy-six children (8.5–10 years, 41 girls and 35 boys) and 45 women (23–30 years) were studied. The children comprised subjects born appropriate for gestational age (<30 gestational weeks) (n=22), born SGA at term (n=23), and full-term normal-weight controls (n=31). Among the women, the corresponding figures were, n=10, n=18, and n=17 respectively. Fasting levels of IGFBP1, leptin, insulin, and IGF1 were determined and total adiponectin only in women. RESULTS: In girls and women, term SGA subjects had higher leptin levels in relation to BMI SDS (P=0.042 and P=0.03 respectively). More than half of IGFBP1 variability was explained by leptin and insulin in children. In term SGA women, IGFBP1 level was lower compared with controls (P=0.012) and the regression line of IGFBP1 on insulin was suppressed below −1 s.d. of a reference material. CONCLUSION: Leptin levels were elevated in term SGA girls and women, in particular in adult women, but not found in preterm girls and women. IGFBP1 was lower in term SGA women. In children, leptin and insulin were strong suppressors of IGFBP1. We speculate that higher leptin levels could be a protective event to enhance hepatic insulin sensitivity. |
format | Online Article Text |
id | pubmed-3680956 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioScientifica |
record_format | MEDLINE/PubMed |
spelling | pubmed-36809562013-06-17 Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age Kistner, Anna Vanpée, Mireille Hall, Kerstin Endocr Connect Research OBJECTIVE: Children born small for gestational age (SGA) are at risk for developing type 2 diabetes. Lipodystrophy leads to early type 2 diabetes and leptin reverses the metabolic consequences of the disease. Low IGF-binding protein 1 (IGFBP1) can predict the development of type 2 diabetes. The aim of this study was to determine leptin, insulin, and IGFBP1 in children and adult women born preterm or SGA to evaluate the role of leptin as a compensatory mechanism in insulin resistance development. METHODS: Seventy-six children (8.5–10 years, 41 girls and 35 boys) and 45 women (23–30 years) were studied. The children comprised subjects born appropriate for gestational age (<30 gestational weeks) (n=22), born SGA at term (n=23), and full-term normal-weight controls (n=31). Among the women, the corresponding figures were, n=10, n=18, and n=17 respectively. Fasting levels of IGFBP1, leptin, insulin, and IGF1 were determined and total adiponectin only in women. RESULTS: In girls and women, term SGA subjects had higher leptin levels in relation to BMI SDS (P=0.042 and P=0.03 respectively). More than half of IGFBP1 variability was explained by leptin and insulin in children. In term SGA women, IGFBP1 level was lower compared with controls (P=0.012) and the regression line of IGFBP1 on insulin was suppressed below −1 s.d. of a reference material. CONCLUSION: Leptin levels were elevated in term SGA girls and women, in particular in adult women, but not found in preterm girls and women. IGFBP1 was lower in term SGA women. In children, leptin and insulin were strong suppressors of IGFBP1. We speculate that higher leptin levels could be a protective event to enhance hepatic insulin sensitivity. BioScientifica 2013-01-25 /pmc/articles/PMC3680956/ /pubmed/23781317 http://dx.doi.org/10.1530/EC-12-0071 Text en © 2012 The Authors. Published by BioScientifica Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Kistner, Anna Vanpée, Mireille Hall, Kerstin Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title | Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title_full | Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title_fullStr | Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title_full_unstemmed | Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title_short | Leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
title_sort | leptin may enhance hepatic insulin sensitivity in children and women born small for gestational age |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680956/ https://www.ncbi.nlm.nih.gov/pubmed/23781317 http://dx.doi.org/10.1530/EC-12-0071 |
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