title: Isolated hyperglycemia at 1 hour on oral glucose tolerance test in pregnancy resembles gestational diabetes mellitus in predicting postpartum metabolic dysfunction.
abstract: OBJECTIVE
  Gestational impaired glucose tolerance (GIGT), defined by a single abnormal value on antepartum 3-h oral glucose tolerance test (OGTT), is a metabolically heterogeneous disorder. Indeed, the antepartum metabolic phenotype of women with a single abnormal value at 1 h during the OGTT (1-h GIGT) resembles that of women with gestational diabetes mellitus (GDM), whereas GIGT at 2 or 3 h (2/3-h GIGT) is similar to normal glucose tolerance (NGT). Thus, we hypothesized that 1-h GIGT would be associated with the same adverse outcomes as GDM, i.e., increased infant birth weight and postpartum metabolic dysfunction.
  
  
  METHODS
  A total of 361 women underwent an antepartum glucose challenge test (GCT) and a 3-h OGTT, assessment of obstetrical outcome at delivery, and metabolic characterization by OGTT at 3 months postpartum. The antepartum GCT/OGTT identified five study groups: GDM (n = 97), 1-h GIGT (n = 28), 2/3-h GIGT (n = 34), abnormal GCT NGT (abnormal GCT with NGT on OGTT) (n = 128), and normal GCT NGT (normal GCT with NGT on OGTT) (n = 74).
  
  
  RESULTS
  Caesarian section rate was higher in women with 1-h GIGT, but birth weight did not differ significantly between the non-GDM groups (P = 0.1978). At 3 months postpartum, glycemia (area under the glucose curve) progressively increased across the groups from normal GCT NGT to abnormal GCT NGT to 2/3-h GIGT to 1-h GIGT to GDM (P < 0.0001), while both insulin sensitivity (IS(OGTT)) and beta-cell function (insulinogenic index/homeostasis model assessment of insulin resistance [HOMA-IR]) progressively decreased (P = 0.002 and P < 0.0001, respectively). The strongest independent negative predictors of insulinogenic index/HOMA-IR were GDM (t = -4.1, P < 0.0001) and 1-h GIGT (t = -3.8, P = 0.0002).
  
  
  CONCLUSIONS
  Like GDM, 1-h GIGT is associated with postpartum glycemia, insulin resistance, and beta-cell dysfunction.
authors: Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Canada. rretnakaran@mtsinai.on.ca
authors: Ravi
authors: R
authors: Retnakaran
authors: Ying
authors: Y
authors: Qi
authors: Mathew
authors: M
authors: Sermer
authors: Philip W
authors: PW
authors: Connelly
authors: Bernard
authors: B
authors: Zinman
authors: Anthony J G
authors: AJ
authors: Hanley
mesh_terms: D000328:Adult; D001724:Birth Weight; D002170:Canada; D002585:Cesarean Section / Q000706:statistics & numerical data; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology*; D016640:Diabetes, Gestational / Q000097:blood* / Q000145:classification; D005260:Female; D020567:Fetal Weight; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000097:blood*; D007231:Infant, Newborn; D050417:Insulin-Secreting Cells / Q000378:metabolism; D008659:Metabolic Diseases / Q000453:epidemiology*; D010298:Parity; D049590:Postpartum Period; D011237:Predictive Value of Tests; D011247:Pregnancy / Q000097:blood*; D012016:Reference Values; D011795:Surveys and Questionnaires; D015430:Weight Gain