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Research

Nutritional Role of Phytochemicals

Master
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Defining a Pathway of Oxalic Acid Catabolism, Influence on Nutritional Composition, Phytochemical, & Production in Plants

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Dietary oxalic acid, consumed primarily through plant-based foods, has been shown to contribute to the formation of kidney stones, decrease the nutritional value of edible plants by acting as an antinutrient, and even exacerbate symptoms associated with other conditions such as autism. The incidence of these negative impacts appears to be rising and will most likely continue to rise with the recommendations for an increase in the consumption of fruits and vegetables. Although dietary oxalic acid has been known to have a negative impact on human health our understanding of the mechanisms regulating its concentration in plant foods is lacking. Recently, we identified an oxalyl-CoA synthetase that is responsible for catalyzing the first step in a previously uncharacterized pathway of oxalate degradation in the plant model Arabidopsis. In this project we will extend this initial finding by first assessing whether this novel pathway of oxalate degradation plays a role in regulating the concentration of oxalate found in selected leafy greens. Second, we will identify and characterize the genes and encoded enzymes responsible for catalyzing each step in this pathway of oxalate catabolism. Third, we will determine the influence of this pathway of oxalate catabolism on the nutritional composition, phytochemical profile, and production characteristics in selected leafy greens. It is anticipated that completion of the proposed basic and applied objectives will result in a gain in knowledge and resources beneficial to a broad range of scientists, producers interested in growing a more healthful food supply, and diet conscious consumers. 

Research Faculty: Paul Nakata

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Effect of Pregnancy and Lactation on Carotenoid Status and Bioactivity

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Carotenoids are red, orange, and yellow pigments in fruits and vegetables, which can contribute to vitamin A requirements, and can act as anti-oxidants and anti-inflammatories. Carotenoids must be obtained from the diet. The fetus acquires carotenoids during gestation, and the infant acquires carotenoids from breast milk or formula. Carotenoids may convey cognitive and anti-inflammatory benefits to both the mother and infant, but whether carotenoids are specifically associated with reduced inflammation or improved cognitive function in pregnant or lactating mothers is unknown. Obese mothers have lower blood and breast milk carotenoid concentrations than lean mothers, but the dietary, body composition, and genetic determinants of this phenomenon are unclear. Understanding the dietary, physiologic, and genetic determinants of maternal carotenoid status is necessary for developing dietary strategies to improve health and quality of life for mothers and infants. The objectives of this project are to define the effect of pregnancy and lactation on carotenoid and vitamin A status and markers of bioactivity in diverse healthy weight and obese women, and to determine the metabolic causes for why greater body fat decreases breast milk and blood carotenoid concentrations in mothers. This project is expected to lead to an improved understanding of the effects of pregnancy and lactation on carotenoid status in healthy, American mothers, the association of maternal carotenoid status with markers of inflammation and cognitive function, and 3) an improved understanding of the absorption and metabolism of carotenoids in obese and normal weight lactating mothers.

Research Faculty: Nancy E. Moran

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'Plant Antinutrients and the Gut Microbiome: A New Dimension

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The goal of this project is to understand the genetic, hormonal, and psychological factors that regulate mammary gland function in lactating mothers and in the maternal-infant interactions. It is well known that obese women struggle to lactate. In Objective 1 we will determine the role of postpartum plasma progesterone in lactation failure in obese women. In Objective 2 we will explore factors that might affect mammary gland development and function in lean and obese mice. These factors include the use of genetically modified mouse models and pharmacological approaches to determine the roles of inflammation, inflammatory cells, and markers of inflammation as well as mineralocorticoids. In addition, we will determine the relationship of maternal oxytocin response and maternal-infant sensitivity, breastfeeding duration and efficacy, and maternal brain response using functional magnetic resonance imaging in obese and non-obese lactating women (Objective 3). The successful completion of these objectives will provide us collectively with new and important insights into the impact of obesity on the pathophysiology of lactation failure by examining many aspects of mammary physiology from secretory activation and function (the role of progesterone and inflammation), and maternal-infant interaction. From these investigations, we anticipate the development of new therapeutic interventions that will positively impact both maternal and infant nutrition and health outcomes by increasing the success of breastfeeding in women who are overweight or obese.

Research Faculty: Kendal Hirschi

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