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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #323350
Research Project: Biology of Obesity Prevention

Location: Healthy Body Weight Research

Title: Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFa expression in Sprague-Dawley rats

Author
item Dekrey, Emilie
item Roemmich, James
item Larson, Kate

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 2/1/2016
Publication Date: 4/1/2016
Citation: Dekrey, E.E., Roemmich, J.N., Claycombe, K.J. 2016. Maternal low protein diet leads to placental angiogenic compensation via dysregulated M1/M2 macrophages and TNFa expression in Sprague-Dawley rats [abstract]. Federation of American Societies for Experimental Biology Conference, April 1-6, 2016, San Diego, California. 30:1169.8.

Interpretive Summary: 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 or 20% 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 placentas had an increase in angiogenic factors, FGF2, VEGFR-1, IGF2, M2 macrophages producing TNFa 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.

Technical 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 or 20% 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 placentas had an increase in angiogenic factors, FGF2, VEGFR-1, IGF2, M2 macrophages producing TNFa 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.