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Reduction Of Adiposity Improves Preeclampsia (PE) Symptoms In BPH/5 Mice
Author(s) -
Lob Heinrich,
Sones Jennifer,
Song Jiunn,
Davisson Robin
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb768
Subject(s) - preeclampsia , medicine , endocrinology , pregnancy , fetus , gestation , gestational hypertension , intrauterine growth restriction , birth weight , adipose tissue , biology , genetics
Preeclampsia (PE) is a hypertensive proteinuric disorder of pregnancy that can result in fetal demise and growth restriction. Although it is a major cause of fetal and maternal morbidity/mortality, the underlying mechanisms remain unclear. Increased adiposity is a risk factor for PE. However, longitudinal studies to investigate the contribution of adiposity to PE are difficult to perform in humans. We utilized the BPH/5 mouse, a spontaneous model of PE, to test the hypothesis that calorie restriction ( cr ) before and during gestation would improve adverse pregnancy outcomes in this model. Food intake was measured in non‐pregnant (NP) BPH/5 and C57 controls. We found that NP BPH/5 are hyperphagic (3.42 ± 0.1 g; C57: 2.91 ± 0.1 g, n=7, P<0.05). Matching food availability for BPH/5 to the amount consumed by C57 significantly reduced NP and late‐gestational (e18.5) gonadal white adipose tissue in BPH/5 (NP: adlib : 0.46 ± 0.06 g, cr : 0.30 ± 0.03 g, n=9‐15, P<0.05; e18.5: adlib : 0.90 ± 0.19 g, cr : 0.33 ± 0.08 g, n=4, P<0.05). This strategy also prevented proteinuria at e18.5 as well as improved fetal outcomes, including litter size (BPH/5 ad‐lib : 4.0 ± 0.6; cr : 6.7 ± 0.3, n=3, P<0.05) and pup weight (BPH/5 ad‐lib : 1.5 ± 0.08 g; cr : 1.9 ± 0.04 g, n=6‐9, P<0.05). These data show that reducing food intake before pregnancy has beneficial effects on maternal and fetal outcomes in this model of PE. These data point towards adiposity playing an important role in the pathogenesis of PE. 12SDG9160019, HL084207, HL63887