title: Insulin resistance in healthy prepubertal twins.
abstract: OBJECTIVE
  To evaluate insulin sensitivity (S(I)) in prepubertal twins and to examine the relation to reduced birth weight, prematurity, and peroxisome proliferator-activated receptor-gamma (PPAR gamma) polymorphism.
  
  
  METHODS
  Fifty twins (birth weight SDS, -0.7 +/- 0.2; gestation, 33.5 +/- 0.5 weeks; and body mass index SDS, -0.04 +/- 0.2) were studied at 8.2 +/- 0.3 years. S(I) was measured by Bergman's minimal model from a 90 minutes frequently sampled intravenous glucose test. Twenty control children (height SDS, -1.7 +/- 0.3; birth weight SDS, -0.3 +/- 0.2; and gestation of 39.2 +/- 0.7 weeks) were also evaluated at 7.0 +/- 0.4 years. The PPAR gamma T-variant polymorphism was evaluated in 41 twins. Values are expressed as mean +/- SEM, or 95% confidence intervals.
  
  
  RESULTS
  S(I) was reduced in twins compared with control subjects, (12.7 [11-15] versus 23.0 [16.8-31.4] 10(-4) min(-1) microU/mL, respectively, P=.005). The reduction in S(I) was independent of prematurity and birth weight and zygosity (P<.0001). There was no difference in S(I), even in twin pairs with >20% difference in birth weight (P=.9). The PPAR gamma heterozygote T-variant polymorphism was present in 7 of 41, with a further reduction in S(I) (P=.03) and a later gestation (P=.03). These twins also had increased fat mass (P=.02) but with similar fat free mass (P=.14).
  
  
  CONCLUSIONS
  Twin children, independent of prematurity or birth weight, had a marked reduction in S(I). To use twins as a model to study the fetal origins of adult diseases for glucose homeostasis is not valid.
authors.affiliation: Liggins Institute, Health Research Council Biostatistics Unit, Department of Community Health, University of Auckland, Auckland, New Zealand.
authors.forename: Craig A
authors.initials: CA
authors.lastname: Jefferies
authors.forename: Paul L
authors.initials: PL
authors.lastname: Hofman
authors.forename: Hans
authors.initials: H
authors.lastname: Knoblauch
authors.forename: Friedrich C
authors.initials: FC
authors.lastname: Luft
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Robinson
authors.forename: Wayne S
authors.initials: WS
authors.lastname: Cutfield
mesh_terms: D016022:Case-Control Studies; D002648:Child; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D004200:Diseases in Twins / Q000453:epidemiology* / Q000235:genetics; D005260:Female; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D009520:New Zealand / Q000453:epidemiology; D011110:Polymorphism, Genetic; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics
chemical_list: D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors