title: Abdominal fat accumulation in adults born preterm exposed antenatally to maternal glucocorticoid treatment is dependent on glucocorticoid receptor gene variation.
abstract: BACKGROUND
  Preterm birth is associated with short stature, abdominal adiposity, insulin resistance, and hypertension, resembling effects of increased glucocorticoid bioactivity. Although antenatal glucocorticoid treatment does not substantially contribute to these associations, it is unknown whether genetic variants in the glucocorticoid receptor gene could modulate the effects of antenatal glucocorticoid treatment on the above phenotype.
  
  
  OBJECTIVE
  Our objective was to test the effects of the R23K and N363S variants, associated with decreased and increased sensitivity to cortisol, respectively, on the metabolic profile in adults born preterm of whom some had been treated with glucocorticoids antenatally and/or in the early postnatal phase.
  
  
  METHODS
  This was a prospective follow-up study that included 263 19-year-olds born at a gestational age under 32 wk from the Dutch Project on Preterm and Small-for-Gestational-Age Infants cohort.
  
  
  METHODS
  This was a nationwide multicenter follow-up study.
  
  
  METHODS
  Adult height and body composition, fasting serum glucose, insulin and cholesterol levels, and blood pressure were evaluated.
  
  
  RESULTS
  At 19 yr of age, waist circumference was 1.67 ± 0.90 sd score in 363S carriers who had been treated antenatally with glucocorticoids (n = 4), which was much higher than that of the other groups (P for interaction = 0.03). A similar association was found for the waist-to-hip ratio sd score (P = 0.03). Similar associations were absent with the R23K polymorphism. There was no interaction between these genotypes and postnatal glucocorticoid treatment on serum levels of glucose, insulin, and cholesterol or blood pressure.
  
  
  CONCLUSIONS
  In prematurely born individuals carrying the 363S variant, antenatal glucocorticoid treatment predisposes to abdominal adiposity at age 19 yr.
authors.affiliation: Department of Pediatric Leiden University Medical Center, 2333 ZA Leiden, The Netherlands. m.finken@vumc.nl
authors.forename: Martijn J J
authors.initials: MJ
authors.lastname: Finken
authors.forename: Ingrid
authors.initials: I
authors.lastname: Meulenbelt
authors.forename: Friedo W
authors.initials: FW
authors.lastname: Dekker
authors.forename: Marijke
authors.initials: M
authors.lastname: Frölich
authors.forename: Frans J
authors.initials: FJ
authors.lastname: Walther
authors.forename: Johannes A
authors.initials: JA
authors.lastname: Romijn
authors.forename: P Eline
authors.initials: PE
authors.lastname: Slagboom
authors.forename: Jan M
authors.initials: JM
authors.lastname: Wit
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism*; D000328:Adult; D001724:Birth Weight / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001823:Body Composition / Q000502:physiology; D001827:Body Height / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D005865:Gestational Age; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000453:epidemiology; D007234:Infant, Premature; D007328:Insulin / Q000097:blood; D009426:Netherlands / Q000453:epidemiology; D010641:Phenotype; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D011965:Receptors, Glucocorticoid / Q000235:genetics* / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D007328:Insulin; D011965:Receptors, Glucocorticoid; D002784:Cholesterol; D006854:Hydrocortisone