title: Programming of adiposity in offspring of mothers with type 1 diabetes at age 7 years.
abstract: OBJECTIVE
  The goals of this study were to examine the influence of maternal type 1 diabetes during pregnancy on offspring adiposity and glucose tolerance at age 7 years and to assess whether metabolic factors at birth (neonatal leptin and insulin) predict adverse outcomes.
  
  
  METHODS
  We examined 100 offspring of mothers with type 1 diabetes (OT1DM) and 45 offspring of control mothers. Mothers had previously been recruited during pregnancy, and, where possible, birth weight, umbilical cord insulin, and leptin were measured. Children were classed as overweight and obese using age-specific reference ranges.
  
  
  RESULTS
  OT1DM had similar height (control, 1.25 +/- 0. 06 m; OT1DM, 1.24 +/- 0.06 m; P = 0.81) but were heavier (control, 25.5 +/- 3.8 kg; OT1DM, 27.1 +/- 5.7 kg; P = 0.048) and had an increased BMI (control, 16.4 kg/m(2); OT1DM, 17.4 +/- 2.6 kg/m(2), P = 0.005). Waist circumference (control, 56.0 +/- 3.7 cm; OT1DM, 58 +/- 6.8 cm; P = 0.02) and sum of skinfolds were increased (control, 37.5 +/- 17.0 mm [n = 42]; OT1DM, 46.1 +/- 24.2 mm [n = 91]; P = 0.02), and there was a marked increase in the prevalence of overweight and obese children (OT1DM, 22% overweight and 12% obese; control, 0% overweight and 7% obese; chi(2) P = 0.001). Glucose tolerance was not different compared with that in control subjects. BMI at age 7 years correlated with cord leptin (OT1DM, r = 0.25; n = 61, P = 0.047), weakly with adjusted birth weight (r = 0.19; P = 0.06) and hematocrit (r = 0.25; n = 50, P = 0.07), but not cord insulin (OT1DM, r = -0.08; P = 0.54).
  
  
  CONCLUSIONS
  OT1DM are at increased risk of overweight and obesity in childhood. This risk appears to relate, in part, to fetal leptin and hematocrit but not insulin.
authors.affiliation: Faculty of Medicine, University of Glasgow, Glasgow, UK. r.lindsay@clinmed.gla.ac.uk
authors.forename: Robert S
authors.initials: RS
authors.lastname: Lindsay
authors.forename: Scott M
authors.initials: SM
authors.lastname: Nelson
authors.forename: James D
authors.initials: JD
authors.lastname: Walker
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Greene
authors.forename: Gillian
authors.initials: G
authors.lastname: Milne
authors.forename: Naveed
authors.initials: N
authors.lastname: Sattar
authors.forename: Donald W
authors.initials: DW
authors.lastname: Pearson
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D001724:Birth Weight; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology* / Q000378:metabolism; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005333:Fetus / Q000378:metabolism; D005500:Follow-Up Studies; D018149:Glucose Intolerance / Q000453:epidemiology* / Q000378:metabolism; D006400:Hematocrit; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D009035:Mothers; D009765:Obesity / Q000453:epidemiology* / Q000378:metabolism; D011237:Predictive Value of Tests; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology* / Q000378:metabolism; D015995:Prevalence; D012307:Risk Factors
chemical_list: D007328:Insulin; D020738:Leptin