Reference no: EM133431824
Obesity is a growing public health concern worldwide, particularly among women of reproductive age [1]. Maternal obesity is associated with a range of adverse pregnancy outcomes - it can affect fetal development and program long-term health outcomes in the offspring [1]. The specific mechanisms between maternal obesity and adverse pregnancy outcomes are not fully understood; but may involve excessive inflammation in the placenta [2].
Inflammation is the body's immune response to injury, infection, or other harmful stimuli; however, it is also a critical aspect of a successful pregnancy [2]. Indeed, higher levels of inflammatory cytokines such as IL- 1ß, IL-6, IN-y and TNF-a are observed in the circulation of pregnant women compared to non-pregnant women [3]. On the other hand, excessive levels of inflammation can be harmful [2, 3].
The placenta plays a critical role in pregnancy by facilitating nutrient and gas exchange between the maternal and fetal circulation [41. There is some evidence that maternal obesity may increase inflammation in the placenta, which, in turn, can contribute to development of adverse outcomes [4].
AIM: To compare the level of placental inflammation in obese and normal pregnancy in mid-gestation.
PROJECT: Rats were fed either a control (CON) diet or a cafeteria-style diet (CAF) of human snack foods from 8 weeks prior to and during pregnancy. Consumption of the CAF diet induced obesity by
about 25% prior to pregnancy [5]. Placental tissues were obtained on day 15 of gestation (term = 23
days) from each of these groups. Maternal obesity reduced fetal and placental weight, potentially through placental dysfunction. We will use quantitative PCR to determine whether maternal obesity altered placental tissue inflammatory gene expression in mid-pregnancy.