title: Preterm birth and random plasma insulin levels at birth and in early childhood.
abstract: OBJECTIVE
  Although previous reports have linked preterm birth with insulin resistance in children and adults, it is not known whether altered insulin homeostasis is detectable at birth and tracks from birth through childhood.
  
  
  OBJECTIVE
  To investigate whether preterm birth is associated with elevated plasma insulin levels at birth and whether this association persists into early childhood.
  
  
  METHODS
  A prospective birth cohort of 1358 children recruited at birth from 1998 to 2010 and followed-up with prospectively from 2005 to 2012 at the Boston Medical Center in Massachusetts.
  
  
  METHODS
  Random plasma insulin levels were measured at 2 time points: at birth (cord blood) and in early childhood (venous blood). The median age was 1.4 years (interquartile range [IQR], 0.8-3.3) among 4 gestational age groups: full term (≥39 wk), early term (37-38 wk), late preterm (34-36 wk), and early preterm (<34 wk).
  
  
  RESULTS
  The geometric mean of insulin levels at birth were 9.2 µIU/mL (95% CI, 8.4-10.0) for full term; 10.3 µIU/mL (95% CI, 9.3-11.5) for early term; 13.2 µIU/mL (95% CI, 11.8-14.8) for late preterm; and 18.9 µIU/mL (95% CI, 16.6-21.4) for early preterm. In early childhood, these levels were 11.2 µIU/mL (95% CI, 10.3-12.0) for full term; 12.4 µIU/mL (95% CI, 11.3-13.6) for early term; 13.3 µIU/mL (95% CI, 11.9-14.8) for late preterm; and 14.6 µIU/mL (95% CI, 12.6-16.9) for early preterm. Insulin levels at birth were higher by 1.13-fold (95% CI, 0.97-1.28) for early term, 1.45-fold (95% CI, 1.25-1.65) for late preterm, and 2.05-fold (95% CI, 1.69-2.42) for early preterm than for those born full term. In early childhood, random plasma insulin levels were 1.12-fold (95% CI, 0.99-1.25) higher for early term, 1.19-fold (95% CI, 1.02-1.35) for late preterm, and 1.31-fold (95% CI, 1.10-1.52) for early preterm than those born full term. The association was attenuated after adjustment for postnatal weight gain and was not significant after adjustment for insulin levels at birth. Infants ranked in the top insulin tertile at birth were more likely to remain in the top tertile (41.2%) compared with children ranked in the lowest tertile (28.6%) in early childhood.
  
  
  CONCLUSIONS
  There was an inverse association between gestational age and elevated plasma insulin levels at birth and in early childhood. The implications for future development of insulin resistance and type 2 diabetes warrant further investigation.
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Guoying
authors: G
authors: Wang
authors: Division of Endocrinology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland.
authors: Sara
authors: S
authors: Divall
authors: Division of Endocrinology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland.
authors: Sally
authors: S
authors: Radovick
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: David
authors: D
authors: Paige
authors: Division of Epidemiology, Department of Family Medicine and Population Health, Virginia Commonwealth University School of Medicine, Richmond.
authors: Yi
authors: Y
authors: Ning
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Zhu
authors: Z
authors: Chen
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Yuelong
authors: Y
authors: Ji
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Xiumei
authors: X
authors: Hong
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Sheila O
authors: SO
authors: Walker
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Deanna
authors: D
authors: Caruso
authors: Department of Pediatrics, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts.
authors: Colleen
authors: C
authors: Pearson
authors: Department of Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
authors: Mei-Cheng
authors: MC
authors: Wang
authors: Department of Pediatrics, Boston University School of Medicine and Boston Medical Center, Boston, Massachusetts.
authors: Barry
authors: B
authors: Zuckerman
authors: Division of General Pediatrics and Adolescent Medicine, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland.
authors: Tina L
authors: TL
authors: Cheng
authors: Department of Population, Family and Reproductive Health, Center on Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland6Division of General Pediatrics and Adolescent Medicine, Department of Pediat.
authors: Xiaobin
authors: X
authors: Wang
mesh_terms: D002675:Child, Preschool; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D005865:Gestational Age; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D047928:Premature Birth; D012306:Risk; D014481:United States / Q000453:epidemiology
chemical_list: D007328:Insulin