title: Low birthweight and premature birth are both associated with type 2 diabetes in a random sample of middle-aged Danes.
abstract: OBJECTIVE
  We studied the associations of size at birth and prematurity with type 2 diabetes, insulin sensitivity and beta cell function in the Danish population-based Inter99 study (ClinicalTrials.gov NCT00289237).
  
  
  METHODS
  Information about size at birth and prematurity was identified from original midwife records in 4,744 middle-aged Danes. Type 2 diabetes status, insulin sensitivity (Matsuda index) and beta cell function (disposition index) were assessed using a 75 g oral glucose tolerance test. Participants born prematurely were compared with a group of at-term participants born small for gestational age.
  
  
  RESULTS
  An increase in birthweight of 1 kg was associated with a 51% (OR 0.49, 95% CI 0.35-0.69) reduced risk of type 2 diabetes. Ponderal index, reflecting thinness at birth, was associated with type 2 diabetes to the same extent as birthweight. The prevalence of type 2 diabetes was increased to a similar degree in participants born prematurely and participants born small for gestational age, although the former had a higher ponderal index at birth. In addition, birthweight z-scores, reflecting fetal growth rate, were unrelated to the risk of type 2 diabetes and to other measures of glucose regulation in participants born prematurely. While low birthweight was inversely associated with insulin sensitivity and beta cell function, prematurity was associated solely with decreased insulin sensitivity.
  
  
  CONCLUSIONS
  While the association between birthweight and risk of type 2 diabetes is mediated via combined effects on beta cell function and insulin sensitivity, prematurity seems to influence risk of type 2 diabetes via attenuated insulin sensitivity only and independently of fetal growth rates.
authors.affiliation: Steno Diabetes Center, Niels Steensens Vej 1, 2820 Gentofte, Denmark. kapg@steno.dk
authors.forename: K
authors.initials: K
authors.lastname: Pilgaard
authors.forename: K
authors.initials: K
authors.lastname: Færch
authors.forename: B
authors.initials: B
authors.lastname: Carstensen
authors.forename: P
authors.initials: P
authors.lastname: Poulsen
authors.forename: C
authors.initials: C
authors.lastname: Pisinger
authors.forename: O
authors.initials: O
authors.lastname: Pedersen
authors.forename: D R
authors.initials: DR
authors.lastname: Witte
authors.forename: T
authors.initials: T
authors.lastname: Hansen
authors.forename: T
authors.initials: T
authors.lastname: Jørgensen
authors.forename: A
authors.initials: A
authors.lastname: Vaag
mesh_terms: D000328:Adult; D001724:Birth Weight / Q000502:physiology; D003718:Denmark / Q000453:epidemiology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D018149:Glucose Intolerance / Q000453:epidemiology; D006801:Humans; D007230:Infant, Low Birth Weight / Q000502:physiology; D007231:Infant, Newborn; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000502:physiology; D008875:Middle Aged; D011247:Pregnancy; D047928:Premature Birth / Q000453:epidemiology*; D011897:Random Allocation; D012307:Risk Factors