title: Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India.
abstract: OBJECTIVE
  The association between lower birthweight and metabolic syndrome may result from fetal undernutrition (fetal programming hypothesis) and/or genes causing both low birthweight and insulin resistance (fetal insulin hypothesis). We studied associations between the birthweight of parents and metabolic syndrome in the offspring.
  
  
  METHODS
  We identified men and women (aged 35-68 years), who had been born in Holdsworth Memorial Hospital, Mysore, India. We also identified the offspring (20-46 years) of these men and women. In total, 283 offspring of 193 mothers and 223 offspring of 144 fathers were studied. Investigations included anthropometry, oral glucose tolerance, plasma insulin and lipid concentrations and blood pressure. The metabolic syndrome was defined using WHO criteria.
  
  
  RESULTS
  Among the offspring, lower birthweight was associated with an increased risk of glucose intolerance (impaired glucose tolerance, impaired fasting glucose or type 2 diabetes) and higher cholesterol and triacylglycerol concentrations (p < 0.05 for all adjusted for sex and age). Most outcomes in the offspring, including most individual components of the metabolic syndrome, were unrelated to parental birthweight. However, both maternal and paternal birthweight were inversely related to offspring metabolic syndrome (odds ratio [OR] 0.36 [95% CI: 0.13-1.01] per kg, p = 0.053 for mother-offspring pairs; OR 0.26 [0.07-0.93], p = 0.04 for father-offspring pairs, adjusted for offspring age, sex, BMI and socioeconomic status). Maternal birthweight was inversely related to offspring systolic blood pressure (beta = -2.5 mmHg [-5.00 to 0.03] per kg maternal birthweight; p = 0.052).
  
  
  CONCLUSIONS
  Factors in both parents may influence the risk of metabolic syndrome in their offspring. There are several possible explanations, but the findings are consistent with the fetal insulin (genetic) hypothesis.
authors.affiliation: Holdsworth Memorial Hospital, Mysore, Karnataka, India. hmhhrcr@sancharnet.in
authors.forename: S R
authors.initials: SR
authors.lastname: Veena
authors.forename: S
authors.initials: S
authors.lastname: Geetha
authors.forename: S D
authors.initials: SD
authors.lastname: Leary
authors.forename: J
authors.initials: J
authors.lastname: Saperia
authors.forename: D J
authors.initials: DJ
authors.lastname: Fisher
authors.forename: K
authors.initials: K
authors.lastname: Kumaran
authors.forename: P
authors.initials: P
authors.lastname: Coakley
authors.forename: C E
authors.initials: CE
authors.lastname: Stein
authors.forename: C H D
authors.initials: CH
authors.lastname: Fall
mesh_terms: D000328:Adult; D032721:Adult Children; D000368:Aged; D001724:Birth Weight / Q000235:genetics / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000503:physiopathology; D004777:Environment; D044127:Epigenesis, Genetic; D005220:Fathers; D005260:Female; D018149:Glucose Intolerance / Q000453:epidemiology; D006801:Humans; D007194:India; D007230:Infant, Low Birth Weight / Q000502:physiology; D007231:Infant, Newborn; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology* / Q000208:ethnology / Q000503:physiopathology; D008875:Middle Aged; D009035:Mothers; D012189:Retrospective Studies; D012307:Risk Factors