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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Research Project #436644

Research Project: Epigenetic Regulation of Obesity

Location: Healthy Body Weight Research

Project Number: 3062-51000-054-00-D
Project Type: In-House Appropriated

Start Date: Jun 5, 2019
End Date: Jun 4, 2024

Objective:
Objective 1: Demonstrate effects of parental diet and exercise on placental epigenetic programming that affects offspring obesity and type 2 diabetes mellitus. Objective 2: Determine the effects of maternal dietary patterns on placental tissue epigenetic programming and central dopaminergic control of offspring eating behavior. Objective 3: Define intervention strategies to reverse placental programming induced by parental high-fat diet.

Approach:
The maternal and paternal consumption of excess food energy leading to parental obesity contributes to the subsequent development of offspring obesity. This phenomenon, in part, involves the epigenetic transmission of obesity risk across generations. The overarching hypothesis of this proposal is that a parental high fat diet and sedentary conditions regulate offspring obesity risk via modifying early epigenetic programming of placental tissue. We propose to study how these placental changes result in adipose and skeletal tissues energy metabolism and eating behavior alterations in the offspring. The primary focus of this project will be on placental tissue epigenetic gene expression influencing placental structural alterations and inflammation resulting in maternal nutrient transport dysfunction. Both animal and human studies show that maternal and paternal diets and obesity adversely affect fetal growth by altering placental structure and function, resulting in adverse birth outcomes and offspring obesity. Our preliminary data demonstrate that placental inflammation and nutrient transporter gene expressions are influenced by parental diet and exercise. Our new research project is an extension of our current and previous projects in which we demonstrated that maternal low protein and high fat diets increase placental tissue scarring, resulting in neovascularization and inflammation that increase offspring obesity and type 2 diabetes mellitus (T2DM) risks. There is little research on how maternal and paternal diets and exercise influence offspring obesity and T2DM risks via epigenetic-induced alterations in placental tissue function. Research results from this project will advance the field of Nutritional Programming in relation to prevention of offspring obesity.