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United States Department of Agriculture

Agricultural Research Service

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Location: Children's Nutrition Research Center

2013 Annual Report

1a. Objectives (from AD-416):
It has now been convincingly demonstrated by human epidemiological investigations that the origins of many of the major chronic diseases that are manifest in adult life have their origins during development. Additionally, molecular, cellular and animal studies have now shown conclusively that interference with, or alteration of, developmental pathways during critical windows of development can provide the pathophysiological basis for the events that take place later in adult life. Our research attempts to answer the following: 1) differentiate the effects of fetal versus postnatal maternal dietary protein restriction on satellite cell accretion and skeletal muscle mass; 2) determine if impaired catch-up growth upon nutritional rehabilitation is due to aberrant epigenetic mechanisms intrinsic to the satellite cell and/or an absence of the extracellular cues necessary to sufficiently accelerate satellite cell division; 3) develop novel techniques to study amino acid metabolism in conscious mouse models, with special emphasis on hepatic and enteral metabolism; 4)determine the role of urea cycle intermediates in maintaining nitric oxide and ureagenesis during different physiological and pathophysiological conditions; 5) determine gene expression in human lactating mammary epithelium; 6) characterize inbred mouse strains for lactation performance, gene expression, and weight gain among offspring in lean and obese animals, making use of a cross-fostering design where appropriate; 7) study the effect of nutrients on mammary gland development and function in mouse models; define the critical window for effects on mammary gland development and function; 8) elucidate the role of vitamin A in vascular development and hematopoiesis using mouse embryos, in vitro assays, and complementary techniques; and 9) identify target genes downstream of retinoic acid signaling that are required for blood and blood vessel development.

1b. Approach (from AD-416):
These research studies will use various techniques to accomplish the research to be undertaken. Establishing the critical window of development during which an inadequate nutrient supply permanently compromises the growth of the skeletal muscle and to understand the responsible mechanisms is of great importance. Research studies will focus on the satellite cell in animal models in order to understand how the nutrition of the fetus and infant has lifelong consequences for the health of the individual. Studies will take place on the role of amino acids in the urea cycle (crucial for nitric oxide synthesis), which is in demand for physiological (growth, pregnancy) and pathophysiological (trauma, sepsis) conditions. Lactation research will be conducted in mouse models to obtain an improved understanding of the genomic factors regulating mammary gland function that is central to providing therapeutic interventions that can aid women to establish and maintain a productive lactation. Since the abnormal formation of blood and blood vessels in adults is central to the progression of prevalent pathologies, including atherosclerosis, tumor angiogenesis, and anemia, researchers will develop an understanding of the cellular and molecular regulation of blood and blood vessel formation. Scientists will study retinoids in their role in the formation and maturation of blood vessels, as well as hematopoiesis, during embryonic development. Additionally, CNRC researchers will investigate, on a cellular and molecular level, the role of retinoid signaling in the regulation of these processes.

3. Progress Report:
Significant research progress was accomplished during the year. To review the progress, please refer to project 6250-51000-054-10S (Project 1), 6250-51000-054-20S (Project 2), and 6250-51000-054-30S (Project 3).

4. Accomplishments

Review Publications
Yazndani, P., Lin, Y., Raman, V., Haymond, M.W. 2012. A single sample GnRHa stimulation test in the diagnosis of precocious puberty. International Journal of Pediatric Endocrinology. 23:1-6.

Haymond, M., Kappelgaard, A., Czernichow, P., Biller, B.M., Takano, K., Kiess, W. 2013. Early recognition of growth abnormalities permitting early intervention. Acta Paediatrica. 102(8):787-796.

Chacko, S.K., Haymond, M.W., Sun, Y., Marini, J.C., Sauer, P.J., Ma, X., Sunehag, A.L. 2012. Effect of ghrelin on glucose regulation in mice. American Journal of Physiology - Endocrinology and Metabolism. 302(9):E1055-E1062.

Marini, J.C. 2012. Arginine and ornithine are the main precursors for citrulline synthesis in mice. Journal of Nutrition. 142:572-580.

Mohammad, M.A., Hadsell, D.L., Haymond, M.W. 2012. Gene regulation of UDP-galactose synthesis and transport: Potential rate limiting processes in initiation of milk production in humans. American Journal of Physiology - Endocrinology and Metabolism. 303(3): E365-E376.

Bacha, F., Pyle, L., Nadeau, K., Cuttler, L., Goland, R., Haymond, M., Levitsky, L., Lynch, J., Weinstock, R.S., White, N.H., Caprio, S., Arslanian, S. 2012. Determinants of glycemic control in youth with type 2 diabetes at randomization in the TODAY study. Pediatric Diabetes. 13(5):377-384.

Hadsell, D.L., Wei, J., Olea, W., Hadsell, L.A., Renwick, A., Thomson, P.C., Shariflou, M. 2012. In "silico" QTL mapping of maternal nurturing ability using the mouse divesity panel. Physiological Genomics. 44(16):787-798.

Bacha, F., Gungor, N., Lee, S., Arslanian, S.A. 2012. Type 2 diabetes in youth: Are there racial differences in beta-cell responsiveness relative to insulin sensitivity? Pediatric Diabetes. 13(3):259-265.

Last Modified: 10/18/2017
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