title: Reduced foetal growth and growth hormone secretion in adult life.
abstract: OBJECTIVE
  Recent studies suggest that growth restriction or other adverse influences acting in utero or during early infancy lead to permanent alterations in growth hormone (GH) secretion. As GH secretion is known to predict cardiovascular risk, alterations in GH may contribute to the association between reduced foetal growth and cardiovascular disease. We have therefore assessed the relationship between birth size and GH secretion in a prospective study of young adults whose birth size was recorded and who have had their current blood pressure and glucose tolerance measured.
  
  
  METHODS
  Prospective cohort study
  
  
  METHODS
  153 healthy men and women, aged 20-21 years.
  
  
  METHODS
  Subjects carried out a timed overnight urinary collection for analysis of GH excretion. Insulin sensitivity and insulin secretion were measured using the intravenous glucose tolerance test with minimal model analysis. Blood pressure, height, weight, usual level of exercise, smoking habits, alcohol consumption, and socio-economic status were also recorded.
  
  
  RESULTS
  GH excretion ranged from 0.01 to 41.8 microU per subject. It did not differ according to gender but was markedly reduced in obese subjects (P < 0.0001) Low birthweight was strongly associated with low GH excretion at age 20 years (P = 0.002). Low placental weight and short body length also predicted low GH (P = 0.02 and P = 0.04, respectively). These relationships were independent of other confounding factors including obesity. GH excretion was not independently related to current levels of blood pressure, insulin sensitivity or insulin secretion.
  
  
  CONCLUSIONS
  Body size at birth predicts GH excretion in adult life. Low GH excretion in people who were small at birth may be one mechanism explaining their increased risk of cardiovascular disease.
authors.affiliation: MRC Metabolic Programming Group, University of Southampton, Southampton General Hospital, Southampton, UK.
authors.forename: D E
authors.initials: DE
authors.lastname: Flanagan
authors.forename: V M
authors.initials: VM
authors.lastname: Moore
authors.forename: I F
authors.initials: IF
authors.lastname: Godsland
authors.forename: R A
authors.initials: RA
authors.lastname: Cockington
authors.forename: J S
authors.initials: JS
authors.lastname: Robinson
authors.forename: D I
authors.initials: DI
authors.lastname: Phillips
mesh_terms: D000328:Adult; D001724:Birth Weight; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology*; D005314:Embryonic and Fetal Development; D005260:Female; D005951:Glucose Tolerance Test; D013006:Growth Hormone / Q000378:metabolism* / Q000652:urine; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D007328:Insulin; D013006:Growth Hormone