title: Cord blood adipokines, neonatal anthropometrics and postnatal growth in offspring of Hispanic and Native American women with diabetes mellitus.
abstract: BACKGROUND
  Offspring of women with diabetes mellitus (DM) during pregnancy have a risk of developing metabolic disease in adulthood greater than that conferred by genetics alone. The mechanisms responsible are unknown, but likely involve fetal exposure to the in utero milieu, including glucose and circulating adipokines. The purpose of this study was to assess the impact of maternal DM on fetal adipokines and anthropometry in infants of Hispanic and Native American women.
  
  
  METHODS
  We conducted a prospective study of offspring of mothers with normoglycemia (Con-O; n = 79) or type 2 or gestational DM (DM-O; n = 45) pregnancies. Infant anthropometrics were measured at birth and 1-month of age. Cord leptin, high-molecular-weight adiponectin (HMWA), pigment epithelium-derived factor (PEDF) and C-peptide were measured by ELISA. Differences between groups were assessed using the Generalized Linear Model framework. Correlations were calculated as standardized regression coefficients and adjusted for significant covariates.
  
  
  RESULTS
  DM-O were heavier at birth than Con-O (3.7 ± 0.6 vs. 3.4 ± 0.4 kg, p = 0.024), but sum of skinfolds (SSF) were not different. At 1-month, there was no difference in weight, SSF or % body fat or postnatal growth between groups. Leptin was higher in DM-O (20.1 ± 14.9 vs. 9.5 ± 9.9 ng/ml in Con-O, p < 0.0001). Leptin was positively associated with birth weight (p = 0.0007) and SSF (p = 0.002) in Con-O and with maternal hemoglobin A1c in both groups (Con-O, p = 0.023; DM-O, p = 0.006). PEDF was positively associated with birth weight in all infants (p = 0.004). Leptin was positively associated with PEDF in both groups, with a stronger correlation in DM-O (p = 0.009). At 1-month, HMWA was positively associated with body weight (p = 0.004), SSF (p = 0.025) and % body fat (p = 0.004) across the cohort.
  
  
  CONCLUSIONS
  Maternal DM results in fetal hyperleptinemia independent of adiposity. HMWA appears to influence postnatal growth. Thus, in utero exposure to DM imparts hormonal differences on infants even without aberrant growth.
authors.affiliation: Department of Pediatrics CMRI Metabolic Research Program, University of Oklahoma Health Sciences Center, 1200 Children's Ave, Suite 4500, Oklahoma City, OK, 73104, USA. april-teague@ouhsc.edu.|Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, 1000 N Lincoln Blvd, Suite 1200, Oklahoma City, OK, 73104, USA. april-teague@ouhsc.edu.
authors.forename: April M
authors.initials: AM
authors.lastname: Teague
authors.affiliation: Department of Pediatrics CMRI Metabolic Research Program, University of Oklahoma Health Sciences Center, 1200 Children's Ave, Suite 4500, Oklahoma City, OK, 73104, USA. david-fields@ouhsc.edu.|Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, 1000 N Lincoln Blvd, Suite 1200, Oklahoma City, OK, 73104, USA. david-fields@ouhsc.edu.
authors.forename: David A
authors.initials: DA
authors.lastname: Fields
authors.affiliation: Department of Pediatrics CMRI Metabolic Research Program, University of Oklahoma Health Sciences Center, 1200 Children's Ave, Suite 4500, Oklahoma City, OK, 73104, USA. chris-aston@ouhsc.edu.
authors.forename: Christopher E
authors.initials: CE
authors.lastname: Aston
authors.affiliation: Department of Pediatrics CMRI Metabolic Research Program, University of Oklahoma Health Sciences Center, 1200 Children's Ave, Suite 4500, Oklahoma City, OK, 73104, USA. kevin-short@ouhsc.edu.|Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, 1000 N Lincoln Blvd, Suite 1200, Oklahoma City, OK, 73104, USA. kevin-short@ouhsc.edu.
authors.forename: Kevin R
authors.initials: KR
authors.lastname: Short
authors.affiliation: Section of Endocrinology and Diabetes, Department of Internal Medicine, University of Oklahoma Health Sciences Center, 1000 N Lincoln Blvd, Suite 2900, Oklahoma City, OK, 73104, USA. t.lyons@qub.ac.uk.|Centre for Experimental Medicine, Queen's University Belfast, Grosvenor Road, Belfast, BT12 6BA, Northern Ireland, UK. t.lyons@qub.ac.uk.
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Lyons
authors.affiliation: Department of Pediatrics CMRI Metabolic Research Program, University of Oklahoma Health Sciences Center, 1200 Children's Ave, Suite 4500, Oklahoma City, OK, 73104, USA. steven-chernausek@ouhsc.edu.|Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, 1000 N Lincoln Blvd, Suite 1200, Oklahoma City, OK, 73104, USA. steven-chernausek@ouhsc.edu.
authors.forename: Steven D
authors.initials: SD
authors.lastname: Chernausek
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D001724:Birth Weight / Q000502:physiology*; D001823:Body Composition / Q000502:physiology; D002657:Child Development / Q000502:physiology*; D016241:Child of Impaired Parents; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005260:Female; D005312:Fetal Blood; D006630:Hispanic or Latino; D006801:Humans; D007198:Indians, North American; D007223:Infant; D007231:Infant, Newborn; D020738:Leptin / Q000097:blood*; D011247:Pregnancy; D011446:Prospective Studies; D055815:Young Adult
chemical_list: D052242:Adiponectin; D020738:Leptin