title: Insulin sensitivity in the offspring of women with type 1 and type 2 diabetes.
abstract: OBJECTIVE
  To determine if insulin sensitivity is altered in prepubertal offspring exposed to a diabetic intrauterine environment.
  
  
  METHODS
  Fifteen control children, 17 offspring of type 1 diabetic women, and 10 offspring of type 2 diabetic women, aged between 5 and 10 years, underwent a frequently sampled intravenous glucose tolerance test (FSIGTT). Weight and height were measured, and body composition was calculated using bioelectrical impedance. Bergman's minimal model was applied to the glucose and insulin measurements to obtain values for insulin sensitivity (Si), acute insulin response (AIR), and glucose effectiveness (Sg).
  
  
  RESULTS
  Si was lowest in the offspring of type 2 diabetic mothers, and AIR was highest in this group, although neither of these changes reached significance (Si, P = 0.2, and AIR, P = 0.3). Offspring of type 2 diabetic mothers had higher BMI SD scores (P = 0.004) and percentage fat mass (P = 0.002) than the children in the other two groups. The BMI SD score and percentage fat mass in the subjects, as well as maternal insulin dose, were negatively correlated with offspring insulin sensitivity.
  
  
  CONCLUSIONS
  Intrauterine exposure to hyperglycemia by itself was not associated with alterations in glucose regulation in prepubertal offspring. Children of mothers with type 2 diabetes, however, were overweight, and they had a tendency for a reduced Si. The combined effect of genetic and postnatal environmental factors, rather than prenatal exposure to hyperglycemia, may place this group at risk for developing impaired glucose tolerance in later life.
authors.affiliation: Liggins Institute, Faculty of Medicine and Health Sciences, The University of Auckland, Auckland, New Zealand. w.hunter@auckland.ac.nz
authors.forename: Wendy A
authors.initials: WA
authors.lastname: Hunter
authors.forename: Tim
authors.initials: T
authors.lastname: Cundy
authors.forename: Diana
authors.initials: D
authors.lastname: Rabone
authors.forename: Paul L
authors.initials: PL
authors.lastname: Hofman
authors.forename: Mark
authors.initials: M
authors.lastname: Harris
authors.forename: Fiona
authors.initials: F
authors.lastname: Regan
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Robinson
authors.forename: Wayne S
authors.initials: WS
authors.lastname: Cutfield
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology; D000328:Adult; D001724:Birth Weight; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D015992:Body Mass Index; D002648:Child; D016241:Child of Impaired Parents; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D005260:Female; D019270:Fructosamine / Q000097:blood; D005951:Glucose Tolerance Test; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology; D007231:Infant, Newborn; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D061389:Insulin, Regular, Pork; D008297:Male; D011247:Pregnancy; D012016:Reference Values
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D061389:Insulin, Regular, Pork; D019270:Fructosamine; C000006:insulin, neutral