Transient catabolic state with reduced IGF-I after antenatal glucocorticoids
Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth. Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma ob...
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Veröffentlicht in: | Pediatric research 2007-09, Vol.62 (3), p.295-300 |
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creator | VERHAEGHE, Johan VANSTAPEL, Florent VAN BREE, Rita VAN HERCK, Erik COOPMANS, Willy |
description | Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth. Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (-48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score 0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. Future research should clarify the role of IGF-I in the protein-catabolic response to GC. |
doi_str_mv | 10.1203/PDR.0b013e318123f72f |
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Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (-48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score <0 than in those with a z score >0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. 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Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (-48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score <0 than in those with a z score >0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. These changes may explain the growth-inhibitory effects of repeated antenatal GC administration. Future research should clarify the role of IGF-I in the protein-catabolic response to GC.</description><subject>Amino Acids - blood</subject><subject>Biological and medical sciences</subject><subject>Birth Weight</subject><subject>Blood Glucose - metabolism</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Female</subject><subject>Fetal Blood - chemistry</subject><subject>Fetus - drug effects</subject><subject>Fetus - physiology</subject><subject>General aspects</subject><subject>Glucocorticoids - pharmacology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Insulin-Like Growth Factor Binding Protein 1 - metabolism</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pregnancy</subject><subject>Premature Birth</subject><issn>0031-3998</issn><issn>1530-0447</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkNFKwzAUhoMobk7fQCQ3eldNetI2vZTp5mCgyLwuSXqila6dSYr49kZWGHh1zsX3_4fzEXLJ2S1PGdy9PLzeMs04IHDJU7BFao_IlGfAEiZEcUymjAFPoCzlhJx5_8kYF5kUp2TCizxNyyyfkvXGqc432AVqVFC6bxtDfVAB6XcTPqjDejBY09VykayosgEdVV3ALsItfW8H05vehcb0Te3PyYlVrceLcc7I2-JxM39K1s_L1fx-nRiQPCRWZ0bF1SrLSrBS6oKLPMtBqJopDcCVrJEViJHTKGwpQbDa8rwAa62GGbnZ9-5c_zWgD9W28QbbVnXYD77Ky_gpL0QExR40rvfeoa12rtkq91NxVv1ZrKLF6r_FGLsa-we9xfoQGrVF4HoElDeqtdGhafyBi_eBlwJ-AfGIfJQ</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>VERHAEGHE, Johan</creator><creator>VANSTAPEL, Florent</creator><creator>VAN BREE, Rita</creator><creator>VAN HERCK, Erik</creator><creator>COOPMANS, Willy</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070901</creationdate><title>Transient catabolic state with reduced IGF-I after antenatal glucocorticoids</title><author>VERHAEGHE, Johan ; VANSTAPEL, Florent ; VAN BREE, Rita ; VAN HERCK, Erik ; COOPMANS, Willy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-fb5cac38faf093f88b71465634ad0ab331a8de07ee5cabe4f98340df1673fffb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Amino Acids - blood</topic><topic>Biological and medical sciences</topic><topic>Birth Weight</topic><topic>Blood Glucose - metabolism</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Female</topic><topic>Fetal Blood - chemistry</topic><topic>Fetus - drug effects</topic><topic>Fetus - physiology</topic><topic>General aspects</topic><topic>Glucocorticoids - pharmacology</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Insulin-Like Growth Factor Binding Protein 1 - metabolism</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pregnancy</topic><topic>Premature Birth</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VERHAEGHE, Johan</creatorcontrib><creatorcontrib>VANSTAPEL, Florent</creatorcontrib><creatorcontrib>VAN BREE, Rita</creatorcontrib><creatorcontrib>VAN HERCK, Erik</creatorcontrib><creatorcontrib>COOPMANS, Willy</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatric research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VERHAEGHE, Johan</au><au>VANSTAPEL, Florent</au><au>VAN BREE, Rita</au><au>VAN HERCK, Erik</au><au>COOPMANS, Willy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transient catabolic state with reduced IGF-I after antenatal glucocorticoids</atitle><jtitle>Pediatric research</jtitle><addtitle>Pediatr Res</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>62</volume><issue>3</issue><spage>295</spage><epage>300</epage><pages>295-300</pages><issn>0031-3998</issn><eissn>1530-0447</eissn><coden>PEREBL</coden><abstract>Glucocorticoid (GC) administration before preterm birth reduces neonatal morbidity but may restrain growth. Here we explored the effect of antenatal GC on nutrient substrates [glucose, FFA, amino acids (AA)], and on IGF-I and IGF-binding protein-1 (IGFBP-1). We analyzed umbilical vein (UV) plasma obtained at birth from 91 preterm newborns that received one course of GC (last exposure 1-1358 h before birth) and 49 newborns that did not. We found that recent GC exposure (-48 h) raised glucose, FFA, and AA concentrations, and the homeostasis model assessment of insulin resistance (HOMA-IR) index, but lowered IGF-I concentrations. The AA surge was greater in newborns with a birth weight z score <0 than in those with a z score >0. Although all AA were transiently increased, the increment was most robust for glutamine and alanine. Shorter duration since GC administration and lower IGF-I concentrations independently predicted AA levels. In conclusion, an antenatal course of GC elicited a transient catabolic state encompassing all nutrient substrates, and a temporary drop in IGF-I concentrations. 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subjects | Amino Acids - blood Biological and medical sciences Birth Weight Blood Glucose - metabolism Fatty Acids, Nonesterified - blood Female Fetal Blood - chemistry Fetus - drug effects Fetus - physiology General aspects Glucocorticoids - pharmacology Homeostasis Humans Infant, Newborn Insulin-Like Growth Factor Binding Protein 1 - metabolism Insulin-Like Growth Factor I - metabolism Male Medical sciences Pregnancy Premature Birth |
title | Transient catabolic state with reduced IGF-I after antenatal glucocorticoids |
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