Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFα expression in Sprague‐Dawley rats

Abstract

A maternal low‐protein (LP) diet results in low birth weight, increased offspring rapid adipose tissue catch‐up growth, adult obesity, and insulin resistance in Sprague‐Dawley rats. The placenta plays key roles in nutrient transport and fetal growth. Placental function is dependent on regulation of immune cell populations and growth and angiogenic factors. Therefore, we hypothesize that a maternal LP diet leads to placental dysfunction through dysregulation of immune cell populations, cytokine production, and growth/angiogenic factors. Obese‐prone Sprague‐Dawley dams were fed 8% LP or20% normal protein diets for 3 weeks prior to breeding and through pregnancy. Maternal LP diet led to a decrease in placental weight and efficiency. LP diet placent as had an increase in angiogenic factors, FGF2, VEGFR‐1, IGF2, M2macrophages producing TNFα and a decrease in M1 macrophages and iNKT cells. These results suggest that prenatal protein restriction forces the placenta to upregulate compensating mechanisms of angiogenesis in order to fulfill the nutrient demands of the fetus.Support or Funding InformationThis work was supported by USDA Agricultural Research Service Project #3062‐51000‐052‐00D.