Premium
Placental insufficiency and leptin programming in two generations of Sprague Dawley rats
Author(s) -
Anderson Cindy M,
Lopez Faye,
Sandeen Ashley R,
Benoit Joseph N
Publication year - 2009
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.23.1_supplement.219.3
Subject(s) - offspring , leptin , medicine , endocrinology , in utero , placental insufficiency , blood pressure , fetus , fetal programming , pregnancy , biology , placenta , obesity , genetics
Placental insufficiency (PI) leads to impaired fetal growth and increased risk for hypertension in mothers and their children in later life. Our lab reported hypoleptinemia in pregnant Sprague‐Dawley rat dams with placental insufficiency associated with intrauterine growth restriction. In this study, we investigated the relationships between leptin levels, growth and hypertension, programmed by PI and maternal hypoleptinemia across two generations. Pregnant rat dams had PI induced via reduced utero‐placental perfusion pressure (RUPP) or sham in controls. F1 offspring were bred for second generation (F2). Systolic blood pressure (SBP) was measured weekly (4‐12 weeks). Whole blood was collected from offspring at 6, 9 and 12 weeks. Plasma leptin levels were determined by EIA. Leptin levels were not significantly different in male offspring groups. Weights and leptin levels were increased in female F1 at 12 weeks of age (p<0.05) compared to control and F2. Compared to control, SBP was significantly increased in F1 across age groups (p < 0.05). F2 SBP was increased over control in males at 9 and 12 weeks and across age groups among females (p<0.05). There were no significant correlations with plasma leptin levels and SBP in offspring groups. Our findings indicate that fetal development during maternal hypoleptinemia led to altered growth patterns in females and was not related to hypertension in offspring exposed to PI