Programming of the Hypothalamus-Pituitary-Adrenal Axis by Very Preterm Birth

Background: Many very preterm (i.e.,

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Published in:Annals of nutrition and metabolism 2017-01, Vol.70 (3), p.170-174
Main Authors: Finken, Martijn J.J., van der Voorn, Bibian, Hollanders, Jonneke J., Ruys, Charlotte A., de Waard, Marita, van Goudoever, Johannes B., Rotteveel, Joost
Format: Article
Language:English
Subjects:
Adipose tissue
Adrenal glands
Babies
Biocompatibility
Biological activity
Blood pressure
Corticotropin-releasing hormone
Cortisol
Cortisone
Defects
Female
Genotype & phenotype
Gestation
Glucocorticoids
Hormones
Humans
Hypothalamic-pituitary-adrenal axis
Hypothalamo-Hypophyseal System - abnormalities
Hypothalamus
Infant, Extremely Premature - physiology
Infant, Newborn
Infants
Insulin
Insulin resistance
Male
Messages
Neonates
Phenotype
Pituitary
Pituitary gland
Pituitary-Adrenal System - abnormalities
Premature birth
Review
Review Article
Social interactions
Steroid 11β-hydroxylase
Stress, Physiological - physiology
Stresses
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container_end_page 174
container_issue 3
container_start_page 170
container_title Annals of nutrition and metabolism
container_volume 70
creator Finken, Martijn J.J.
van der Voorn, Bibian
Hollanders, Jonneke J.
Ruys, Charlotte A.
de Waard, Marita
van Goudoever, Johannes B.
Rotteveel, Joost
description Background: Many very preterm (i.e.,
doi_str_mv 10.1159/000456040
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Conversely, later in life these infants show features of increased glucocorticoid bioactivity, such as abdominal adiposity, insulin resistance, raised blood pressure, shorter stature and internalizing problem behavior. Summary: Studies suggested that very preterm newborns have impairments along multiple levels of the hypothalamus-pituitary-adrenal (HPA) axis. Among the impairment were defects in: (1) the pituitary responsiveness to exogenous corticotropin-releasing hormone, (2) 11β-hydroxylase activity, and (3) the interconversion between cortisol and inert cortisone. There is some evidence suggesting that later in life these infants have an increased basal secretion rate of cortisol and adrenal hyperandrogenism. However, the response to acute (psychosocial) stress was blunted rather than enhanced in them. The mechanisms explaining this switch in HPA axis activity are complex and not yet fully understood. Key Messages: Very preterm newborns have several impairments along the HPA axis that could impede an adequate adrenocortical response to stress or illness. Later in life, these infants are predisposed to increased HPA axis activity, which could partially explain their phenotype.</description><identifier>ISSN: 0250-6807</identifier><identifier>ISBN: 3318060720</identifier><identifier>ISBN: 9783318060720</identifier><identifier>EISSN: 1421-9697</identifier><identifier>EISBN: 3318060739</identifier><identifier>EISBN: 9783318060737</identifier><identifier>DOI: 10.1159/000456040</identifier><identifier>PMID: 28301846</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Adipose tissue ; Adrenal glands ; Babies ; Biocompatibility ; Biological activity ; Blood pressure ; Corticotropin-releasing hormone ; Cortisol ; Cortisone ; Defects ; Female ; Genotype &amp; phenotype ; Gestation ; Glucocorticoids ; Hormones ; Humans ; Hypothalamic-pituitary-adrenal axis ; Hypothalamo-Hypophyseal System - abnormalities ; Hypothalamus ; Infant, Extremely Premature - physiology ; Infant, Newborn ; Infants ; Insulin ; Insulin resistance ; Male ; Messages ; Neonates ; Phenotype ; Pituitary ; Pituitary gland ; Pituitary-Adrenal System - abnormalities ; Premature birth ; Review ; Review Article ; Social interactions ; Steroid 11β-hydroxylase ; Stress, Physiological - physiology ; Stresses</subject><ispartof>Annals of nutrition and metabolism, 2017-01, Vol.70 (3), p.170-174</ispartof><rights>2017 The Author(s)</rights><rights>2017 The Author(s) Published by S. Karger AG, Basel</rights><rights>2017 The Author(s) Published by S. 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Karger AG, Basel 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-ca7fbcb757450d9977273203b501180472d9630605014c1612984c0092387cb23</citedby><cites>FETCH-LOGICAL-c446t-ca7fbcb757450d9977273203b501180472d9630605014c1612984c0092387cb23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/48514867$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/48514867$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,885,27922,27923,58236,58469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28301846$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Finken, Martijn J.J.</creatorcontrib><creatorcontrib>van der Voorn, Bibian</creatorcontrib><creatorcontrib>Hollanders, Jonneke J.</creatorcontrib><creatorcontrib>Ruys, Charlotte A.</creatorcontrib><creatorcontrib>de Waard, Marita</creatorcontrib><creatorcontrib>van Goudoever, Johannes B.</creatorcontrib><creatorcontrib>Rotteveel, Joost</creatorcontrib><title>Programming of the Hypothalamus-Pituitary-Adrenal Axis by Very Preterm Birth</title><title>Annals of nutrition and metabolism</title><addtitle>Ann Nutr Metab</addtitle><description>Background: Many very preterm (i.e., &lt;32 weeks of gestation) newborns fail to mount an adequate adrenocortical response to stress or illness, termed relative adrenal insufficiency. Conversely, later in life these infants show features of increased glucocorticoid bioactivity, such as abdominal adiposity, insulin resistance, raised blood pressure, shorter stature and internalizing problem behavior. Summary: Studies suggested that very preterm newborns have impairments along multiple levels of the hypothalamus-pituitary-adrenal (HPA) axis. Among the impairment were defects in: (1) the pituitary responsiveness to exogenous corticotropin-releasing hormone, (2) 11β-hydroxylase activity, and (3) the interconversion between cortisol and inert cortisone. There is some evidence suggesting that later in life these infants have an increased basal secretion rate of cortisol and adrenal hyperandrogenism. However, the response to acute (psychosocial) stress was blunted rather than enhanced in them. The mechanisms explaining this switch in HPA axis activity are complex and not yet fully understood. 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Later in life, these infants are predisposed to increased HPA axis activity, which could partially explain their phenotype.</description><subject>Adipose tissue</subject><subject>Adrenal glands</subject><subject>Babies</subject><subject>Biocompatibility</subject><subject>Biological activity</subject><subject>Blood pressure</subject><subject>Corticotropin-releasing hormone</subject><subject>Cortisol</subject><subject>Cortisone</subject><subject>Defects</subject><subject>Female</subject><subject>Genotype &amp; phenotype</subject><subject>Gestation</subject><subject>Glucocorticoids</subject><subject>Hormones</subject><subject>Humans</subject><subject>Hypothalamic-pituitary-adrenal axis</subject><subject>Hypothalamo-Hypophyseal System - abnormalities</subject><subject>Hypothalamus</subject><subject>Infant, Extremely Premature - physiology</subject><subject>Infant, Newborn</subject><subject>Infants</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Male</subject><subject>Messages</subject><subject>Neonates</subject><subject>Phenotype</subject><subject>Pituitary</subject><subject>Pituitary gland</subject><subject>Pituitary-Adrenal System - abnormalities</subject><subject>Premature birth</subject><subject>Review</subject><subject>Review Article</subject><subject>Social interactions</subject><subject>Steroid 11β-hydroxylase</subject><subject>Stress, Physiological - physiology</subject><subject>Stresses</subject><issn>0250-6807</issn><issn>1421-9697</issn><isbn>3318060720</isbn><isbn>9783318060720</isbn><isbn>3318060739</isbn><isbn>9783318060737</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><recordid>eNpdkc1vEzEQxc2XaFo4cAe0EpdyWJjxty9IoSotUiRyAK4r78ZJNuyuU9uLyH-Pq5SlcBqN3s9Pb_wIeYHwDlGY9wDAhQQOD8gpY6hBgmLmIZkhp1gaadSjvwKFx2QGVEApNagTchrjDgCp5uIpOaGaAWouZ2SxDH4TbN-3w6bw6yJtXXF92Pu0tZ3tx1gu2zS2yYZDOV8FN9iumP9qY1Efiu8uHIplcMmFvvjYhrR9Rp6sbRfd87t5Rr59uvx6cV0uvlx9vpgvyoZzmcrGqnXd1EooLmBljFJUMQqsFoA5PVd0ZSTLV-SdNyiRGs0bAEOZVk1N2Rn5cPTdj3XvVo0bUrBdtQ9tn4NW3rbVv8rQbquN_1kJgZKjyAbndwbB34wupqpvY-O6zg7Oj7FCrbRGo43J6Jv_0J0fQ_6HTBmGFCWlMlNvj1QTfIzBracwCNVte9XUXmZf308_kX9KycDLI_DDho0LEzC9f3WUdzH5e6oWyLVU7Dc86aBd</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Finken, Martijn J.J.</creator><creator>van der Voorn, Bibian</creator><creator>Hollanders, Jonneke J.</creator><creator>Ruys, Charlotte A.</creator><creator>de Waard, Marita</creator><creator>van Goudoever, Johannes B.</creator><creator>Rotteveel, Joost</creator><general>S. 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Conversely, later in life these infants show features of increased glucocorticoid bioactivity, such as abdominal adiposity, insulin resistance, raised blood pressure, shorter stature and internalizing problem behavior. Summary: Studies suggested that very preterm newborns have impairments along multiple levels of the hypothalamus-pituitary-adrenal (HPA) axis. Among the impairment were defects in: (1) the pituitary responsiveness to exogenous corticotropin-releasing hormone, (2) 11β-hydroxylase activity, and (3) the interconversion between cortisol and inert cortisone. There is some evidence suggesting that later in life these infants have an increased basal secretion rate of cortisol and adrenal hyperandrogenism. However, the response to acute (psychosocial) stress was blunted rather than enhanced in them. The mechanisms explaining this switch in HPA axis activity are complex and not yet fully understood. Key Messages: Very preterm newborns have several impairments along the HPA axis that could impede an adequate adrenocortical response to stress or illness. Later in life, these infants are predisposed to increased HPA axis activity, which could partially explain their phenotype.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>28301846</pmid><doi>10.1159/000456040</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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identifier ISSN: 0250-6807
ispartof Annals of nutrition and metabolism, 2017-01, Vol.70 (3), p.170-174
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1421-9697
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source JSTOR Archival Journals
subjects Adipose tissue
Adrenal glands
Babies
Biocompatibility
Biological activity
Blood pressure
Corticotropin-releasing hormone
Cortisol
Cortisone
Defects
Female
Genotype & phenotype
Gestation
Glucocorticoids
Hormones
Humans
Hypothalamic-pituitary-adrenal axis
Hypothalamo-Hypophyseal System - abnormalities
Hypothalamus
Infant, Extremely Premature - physiology
Infant, Newborn
Infants
Insulin
Insulin resistance
Male
Messages
Neonates
Phenotype
Pituitary
Pituitary gland
Pituitary-Adrenal System - abnormalities
Premature birth
Review
Review Article
Social interactions
Steroid 11β-hydroxylase
Stress, Physiological - physiology
Stresses
title Programming of the Hypothalamus-Pituitary-Adrenal Axis by Very Preterm Birth
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