title: Components of the insulin resistance syndrome in seven-year-old children: relations with birth weight and the polyunsaturated fatty acid content of umbilical cord plasma phospholipids.
abstract: OBJECTIVE
  According to the foetal origins hypothesis, there is a relation between foetal nutrition and adult glucose intolerance. In adults, insulin resistance has been associated with dietary polyunsaturated fatty acids. We examined whether the availability of polyunsaturated fatty acids during foetal life, as indicated by the fatty acid composition of cord blood samples, relates to childhood body composition and glycaemic control.
  
  
  METHODS
  Fatty acid concentrations in umbilical cord blood were determined by gas-liquid chromatography in a birth-cohort of infants. When the children were seven years old, fasting glucose, insulin, proinsulin, and leptin levels were measured in 259 of these children, and relations with cord plasma fatty acid concentrations were studied.
  
  
  RESULTS
  Cord plasma phospholipid gamma-linolenic acid and dihomo- gamma-linolenic acid concentrations were negatively related to insulin concentrations and calculated insulin resistance (homeostasis model assessment) at seven years of age. The gamma-linolenic acid concentrations were also negatively related to body fatness and proinsulin and leptin concentrations at seven years of age. No association was found for other polyunsaturated fatty acid concentrations at birth. Adjusted for age, sex, current weight, and gestational age, a lower birth weight related to higher values of insulin resistance variables. The highest insulin concentrations were found in children with a low birth weight and a low gamma-linolenic acid concentration at birth. The relations between gamma-linolenic acid concentration at birth and fasting insulin and calculated insulin resistance remained statistically significant when adjusted for birth weight.
  
  
  CONCLUSIONS
  These findings indicate that foetal availability or metabolism of gamma-linolenic acid could be involved in the early origins of insulin resistance.
authors.affiliation: Department of Human Biology, Maastricht University, Maastricht, The Netherlands.
authors.forename: P
authors.initials: P
authors.lastname: Rump
authors.forename: C
authors.initials: C
authors.lastname: Popp-Snijders
authors.forename: R J
authors.initials: RJ
authors.lastname: Heine
authors.forename: G
authors.initials: G
authors.lastname: Hornstra
mesh_terms: D000328:Adult; D001724:Birth Weight; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D016009:Chi-Square Distribution; D002648:Child; D015331:Cohort Studies; D003920:Diabetes Mellitus / Q000235:genetics; D005314:Embryonic and Fetal Development; D005190:Family; D005231:Fatty Acids, Unsaturated / Q000097:blood*; D005312:Fetal Blood / Q000737:chemistry*; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D009426:Netherlands; D010743:Phospholipids / Q000097:blood*; D011384:Proinsulin / Q000097:blood
chemical_list: D001786:Blood Glucose; D005231:Fatty Acids, Unsaturated; D007328:Insulin; D010743:Phospholipids; D011384:Proinsulin