Effect of lactation on maternal postpartum cardiac function and adiposity

A murine model

Aaron T. Poole, Kathleen Vincent, Gayle Olson, Igor Patrikeev, George Saade, Alison Stuebe, Egle Bytautiene

Research output: Contribution to journalArticle

18 Citations (Scopus)

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. Study Design 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.

Conclusion Our data provide evidence that interruption of lactation adversely affects postpartum maternal cardiovascular function and adiposity.

Original languageEnglish (US)
Pages (from-to)424.e1-424.e7
JournalAmerican Journal of Obstetrics and Gynecology
Volume211
Issue number4
DOIs
StatePublished - Oct 1 2014

Fingerprint

Adiposity
Lactation
Postpartum Period
Mothers
Blood Pressure
Intra-Abdominal Fat
Subcutaneous Fat
Cardiac Output
Metabolic Diseases
Mitral Valve
Stroke Volume
Tomography
Parturition
Students
Hypertension

Keywords

  • adipose
  • blood pressure
  • CD-1 mouse
  • lactation
  • maternal health

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Effect of lactation on maternal postpartum cardiac function and adiposity : A murine model. / Poole, Aaron T.; Vincent, Kathleen; Olson, Gayle; Patrikeev, Igor; Saade, George; Stuebe, Alison; Bytautiene, Egle.

In: American Journal of Obstetrics and Gynecology, Vol. 211, No. 4, 01.10.2014, p. 424.e1-424.e7.

Research output: Contribution to journalArticle

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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. Study Design 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.Conclusion Our data provide evidence that interruption of lactation adversely affects postpartum maternal cardiovascular function and adiposity.",
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AU - Saade, George

AU - Stuebe, Alison

AU - Bytautiene, Egle

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N2 - 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. Study Design 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.Conclusion Our data provide evidence that interruption of lactation adversely affects postpartum maternal cardiovascular function and adiposity.

AB - 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. Study Design 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.Conclusion Our data provide evidence that interruption of lactation adversely affects postpartum maternal cardiovascular function and adiposity.

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