title: Effect of lactation on maternal postpartum cardiac function and adiposity: a murine model.
abstract: OBJECTIVE
  Lactation is associated with reduction in maternal metabolic disease and hypertension later in life; however, findings in humans may be confounded by socioeconomic factors. We sought to determine the independent contribution of lactation on cardiovascular parameters and adiposity in a murine model.
  
  
  METHODS
  Following delivery, CD-1 female mice were randomly divided into 2 groups: lactated (L; nursed pups for 3 weeks, n = 10), and nonlactated (NL; pups were removed after birth, n = 12). Blood pressure (BP) was assessed prepregnancy and at 1 and 2 months' postpartum. Visceral and subcutaneous adipose tissue determined by computed tomography and left ventricular ejection fraction, cardiac output, and the E/A ratio determined by microultrasound were evaluated at 1 and 2 months' postpartum. The results were analyzed using a Student t test (significance at P < .05).
  
  
  RESULTS
  We observed a significantly different maternal BP at 2 months' postpartum with relatively greater BP in NL (systolic BP: NL, 122.2 ± 7.2 vs L, 96.8 ± 9.8 mm Hg; P = .04; diastolic BP: NL, 87.0 ± 6.8 vs L, 65.9 ± 6.2 mm Hg; P = .04). Visceral adipose tissue was significantly increased in NL mice at 1 (22.0 ± 4.1% vs 10.7 ± 1.8%, P = .04) and 2 months' postpartum (22.9 ± 3.5% vs 11.2 ± 2.2%, P = .02), whereas subcutaneous adipose tissue did not differ between the groups. At 2 months' postpartum, ejection fraction (51.8 ± 1.5% vs 60.5 ± 3.8%; P = .04), cardiac output (14.2 ± 1.0 vs 18.0 ± 1.3 mL/min; P = .02) and mitral valve E/A ratio (1.38 ± 0.06 vs 1.82 ± 0.13; P = .04) were significantly lower in NL mice than L mice.
  
  
  CONCLUSIONS
  Our data provide evidence that interruption of lactation adversely affects postpartum maternal cardiovascular function and adiposity.
authors.affiliation: Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX.
authors.forename: Aaron T
authors.initials: AT
authors.lastname: Poole
authors.affiliation: Division of Gynecology, Department of Obstetrics and Gynecology, Center for Biomedical Engineering, University of Texas Medical Branch, Galveston, TX.
authors.forename: Kathleen L
authors.initials: KL
authors.lastname: Vincent
authors.affiliation: Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX.
authors.forename: Gayle L
authors.initials: GL
authors.lastname: Olson
authors.affiliation: Center for Biomedical Engineering, University of Texas Medical Branch, Galveston, TX.
authors.forename: Igor
authors.initials: I
authors.lastname: Patrikeev
authors.affiliation: Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX.
authors.forename: George R
authors.initials: GR
authors.lastname: Saade
authors.affiliation: Department of Obstetrics and Gynecology, University of North Carolina School of Medicine, Chapel Hill, NC.
authors.forename: Alison
authors.initials: A
authors.lastname: Stuebe
authors.affiliation: Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX.
authors.forename: Egle
authors.initials: E
authors.lastname: Bytautiene
mesh_terms: D052436:Adipose Tissue, White / Q000502:physiology; D050154:Adiposity / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D005260:Female; D007774:Lactation / Q000502:physiology*; D051379:Mice; D011897:Random Allocation; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*
keywords: CD-1 mouse; adipose; blood pressure; lactation; maternal health