title: Pancreatic beta-cell function and fetal growth in gestational impaired glucose tolerance.
abstract: OBJECTIVE
  To investigate the metabolic phenotype and pregnancy outcomes of gestational impaired glucose tolerance (IGT) defined by isolated hyperglycemia during an oral glucose tolerance test (OGTT).
  
  
  METHODS
  Retrospective cohort study.
  
  
  METHODS
  University referral hospital.
  
  
  METHODS
  A total of 4,789 women were screened for gestational diabetes mellitus (GDM) between 1996 and 2008 with a glucose challenge test (GCT), followed by a 2-hour 75-g OGTT if the GCT result was abnormal; in addition, measurement of plasma insulin concentration during the OGTT was implemented from 2004.
  
  
  METHODS
  The insulin sensitivity (IS(OGTT)) and beta-cell function (insulinogenic index/homeostasis model assessment for insulin resistance) were calculated for 283 women who underwent a diagnostic OGTT between 2004 and 2008. Perinatal complications were examined in 4,789 women who were screened for GDM between 1996 and 2008.
  
  
  METHODS
  Comparison of outcomes among women stratified by glucose tolerance status using the GCT and OGTT profiles.
  
  
  RESULTS
  Insulin sensitivity and beta-cell function significantly decreased from normal OGTT to 2-hour IGT (single hyperglycemia at 2 hours) to 1-hour IGT (single hyperglycemia at 1 hour) to GDM, with significant differences between normal OGTT and 1-hour IGT or GDM. The occurrence of large-for-gestational age (LGA) neonates was significantly increased in women with GDM or 1-hour IGT (adjusted odds ratio: 2.15, 2.22; 95% confidence interval 1.23-3.75 and 1.04-4.35, respectively) compared to those with normal GCT or normal diagnostic OGTT results.
  
  
  CONCLUSIONS
  Like GDM, isolated 1-hour hyperglycemia on the OGTT is associated with beta-cell dysfunction and an increased risk for LGA neonates.
authors.affiliation: Department of Obstetrics and Gynecology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, Japan. kei@sc.itc.keio.ac.jp
authors.forename: Kei
authors.initials: K
authors.lastname: Miyakoshi
authors.forename: Mamoru
authors.initials: M
authors.lastname: Tanaka
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Saisho
authors.forename: Akira
authors.initials: A
authors.lastname: Shimada
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Minegishi
authors.forename: Seon Hye
authors.initials: SH
authors.lastname: Kim
authors.forename: Satoshi
authors.initials: S
authors.lastname: Asai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Itoh
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Yoshimura
mesh_terms: D000328:Adult; D044466:Asian People; D001786:Blood Glucose / Q000032:analysis; D016640:Diabetes, Gestational / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005320:Fetal Macrosomia / Q000378:metabolism; D018149:Glucose Intolerance / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism*; D007231:Infant, Newborn; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000175:diagnosis / Q000378:metabolism; D011256:Pregnancy Outcome; D012189:Retrospective Studies
chemical_list: D001786:Blood Glucose