title: Insulin resistance in Hispanic large-for-gestational-age neonates at birth.
abstract: BACKGROUND
  Intrauterine exposure to maternal diabetes and large size at birth are known risk factors for the subsequent development of insulin resistance and metabolic syndrome. Although Hispanic youth have been shown to have a high prevalence of metabolic syndrome, it is unknown whether metabolic abnormalities and a predisposition for glucose intolerance are present at birth.
  
  
  OBJECTIVE
  The objective of the study was to determine whether abnormalities in insulin sensitivity exist at or soon after birth in large-for-gestational-age neonates born to Hispanic women with and without gestational diabetes. DESIGN/PATIENTS/SETTING: Forty-two term Hispanic neonates were enrolled for cross-sectional studies at 24-48 h after birth and included nine large-for-gestational-age neonates delivered of women with gestational diabetes (large-for-gestational-age-IDM), 12 large-for-gestational-age but not IDM neonates, 11 poorly grown (at the fifth to 10th percentile), and 10 appropriate-for-gestational-age neonates. Insulin sensitivity and secretion were measured by shortened fasting iv glucose tolerance test.
  
  
  METHODS
  Insulin sensitivity index was measured within 48 h of birth.
  
  
  RESULTS
  Neonates were studied at 36 +/- 11 h postnatally, and all groups were euglycemic at the time of study. However, insulin sensitivity was significantly lower (P < 0.05, ANOVA) in large-for-gestational-age-IDM [3.0 +/- 0.7 (sem) mU/liter.min] and large-for-gestational-age-non-IDM (2.2 +/- 0.4 mU/liter.min) cohorts in comparison with poorly grown (5.0 +/- 0.7 mU/liter.min) and appropriate-for-gestational-age controls (5.4 +/- 0.8 mU/liter.min). Insulin secretion did not differ between groups.
  
  
  CONCLUSIONS
  Reduced insulin sensitivity is present soon after birth in Hispanic large-for-gestational-age neonates born to mothers with and without gestational diabetes, demonstrating the onset of insulin resistance before birth and evidence of altered fetal programming.
authors.affiliation: Department of Pediatrics, Division of Endocrinology, The Ohio State University, 700 Children's Drive, W322, Columbus, Ohio 43205, USA. dyerj@pediatrics.ohio-state.edu
authors.forename: Jennifer Shine
authors.initials: JS
authors.lastname: Dyer
authors.forename: Charles R
authors.initials: CR
authors.lastname: Rosenfeld
authors.forename: Julie
authors.initials: J
authors.lastname: Rice
authors.forename: Mark
authors.initials: M
authors.lastname: Rice
authors.forename: Dana S
authors.initials: DS
authors.lastname: Hardin
mesh_terms: D000328:Adult; D001724:Birth Weight; D001786:Blood Glucose; D003430:Cross-Sectional Studies; D016640:Diabetes, Gestational / Q000208:ethnology / Q000378:metabolism; D005260:Female; D005320:Fetal Macrosomia / Q000208:ethnology* / Q000378:metabolism; D005865:Gestational Age; D006630:Hispanic or Latino / Q000706:statistics & numerical data*; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D011247:Pregnancy; D015995:Prevalence; D012307:Risk Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D008055:Lipids