Location: Arkansas Children's Nutrition Center
2013 Annual Report
1)extend to bone cells and other non-liver tissues; and.
2)reversal of insulin resistance in bone contributes to the protection soy diets provide toward preventing obesity-associated bone loss. Furthermore, the researchers were able to show that the effects of soy diets on bone cells were at least in part associated with phytochemicals found in soy called isoflavones. These data suggest that soy foods and dietary isoflavone supplements may improve bone quality in addition to reducing blood sugar in obese individuals. 9. The effects of soy protein and the soy isoflavone genistein on mammary gland fat cells. Fat cells (adipocytes) are thought to play an important role in breast cancer development and progression. Consumption of soy foods is associated with lower breast cancer rates and lower body fat, but the relationship between soy consumption, mammary gland fat content, and breast cancer has not been established. Researchers at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, found that diets containing soy protein or the soy phytochemical genistein blocked fat cell formation, reduced mammary gland fat content, increased molecules known as tumor suppressors, and blocked cancer-stem cells from progressing toward a cancerous condition in cell culture. These results suggest a potential mechanism by which soy can help prevent breast cancer and may result in the development of a strategy to help prevent the initiation of breast cancer. 10. Soy beans may act to prevent breast cancer. Breast cancer is one of the major chronic diseases of women, and prevention of this disease is much preferred to treatment. Soy food consumption is associated with lower breast cancer rates, but the identity of the active components within soy is still unclear. Two potentially important factors in soybeans are a 43 amino acid peptide (lunasin) and a soy isoflavone (genistein), each of which has been reported to be potential cancer preventive agents. Researchers at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, have studied these compounds to determine if they act through the same mechanisms. Results from this study suggest different mechanisms of action, but the combination of both factors provided increased death (apoptosis) to malignant and non-malignant mammary epithelial cell, actions that are thought to be important in prevention of breast cancer. These results provide potentially important information to help support the use of soy foods in the development of a healthy lifestyle regimen for women at high risk of developing breast cancer. These data also demonstrate that the health effects of food and diets are the result of additive or synergistic actions of many separate food components (phytochemicals, peptides, etc.), and may not be replicated by supplements made from an individual or even several bioactive components. 11. Maternal blueberry consumption may program mammary gland development and risk of breast cancer. Breast cancer is one of the major chronic diseases of women, and environmental exposure (e.g., to dietary factors) is an area of intense research to find either causes or preventions to this disease. Researchers at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, have been studying blueberries because they have been shown to affect metabolism of several organs, including the mammary gland, and these actions could lead to a strategy to prevent breast cancer. They found that maternal consumption of a blueberry-containing diet during pregnancy and lactation reduced tumor size in the mammary gland of offspring genetically predisposed to mammary gland cancer in association with lower serum concentrations of insulin which may also act as a tumor growth factor. Results from this study add to previous results showing how diet can be an important factor in disease prevention. There is an expectation that this can help lead to a dietary strategy that helps reduce breast cancer risks in the future. 12. Saturated fatty acids can lead to inflammation of the placenta. Obesity is associated with low-grade chronic inflammation, which contributes to cellular dysfunction promoting metabolic disease in the offspring. Using an established cell culture model of placental cells, obesity researchers at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, studied the mechanisms by which saturated fatty acids induce inflammation in placenta. These investigators found that saturated fatty acid treatment predominantly altered expression of genes that led to increased inflammation and immediate-early response. These results in cell culture shed new light on how saturated fatty acids and high fat diets may contribute to the development of placental inflammation and dysfunction, and provide an underlying basis for more in-depth studies of human placentas to increase our understanding of how mothers may influence long-term health of their offspring. 13. Maternal obesity is associated with increased inflammation of placentas. Obesity during pregnancy leads to a placental inflammation; however, the underlying causes for obesity-induced placental inflammation in women remain unclear. Recent work in animals by scientists at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, suggests that obese women can program metabolism of their offspring and this may be liked to inflammation. To determine the extent to which inflammatory processes of obese women differed from that of lean women from the Glowing study, metabolic pathways known to produce inflammation were studied in placentas from term pregnancies. Researchers were able to determine that placental inflammation is orchestrated differently by key proteins in placentas from obese women than in lean women, and this may play a role in maternal programming of fetal metabolism. 14. Excess caloric intake recognized as a major source of toxicity. Now that the American Medical Association has declared that obesity is a disease, significantly more attention is being paid to the mechanisms underlying obesity development. There is a need to educate trainees and professionals in both industry and government in the current science underlying obesity. Scientists at the Arkansas Children's Nutrition Center in Little Rock, Arkansas, are at the forefront of new research into molecular mechanisms underlying increased fat accumulation and the health consequences of obesity and were asked to write a new chapter in the sixth edition of the textbook "Casarett & Doull's Toxicology" on the toxic effects of excess calories. This book is the major textbook used by graduate programs in toxicology in the U.S. and is the text used for Board Certification in Toxicology by professionals in industry and government worldwide. Addition of a new chapter on obesity represents recognition that this is a new field of research for the toxicology community and recognition that the ACNC is a leader in this area.
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Crook, T., Armbya, N., Cleves, M., Badger, T.M., Andres, A. 2012. Air displacement plethysmography, dual-energy x-ray absorptiometry, and total body water to evaluate body composition in preschool-age children. Journal of the Academy of Nutrition and Dietetics. 112(12):1993-1998.
Xie, C., Kang, J., Li, Z., Schauss, A.G., Badger, T.M., Nagarajan, S., Wu, T., Wu, X. 2012. The acai flavonoid velutin is a potent anti-inflammatory agent: Blockade of LPS-mediated TNF-alpha and IL-6 production through inhibiting NF-kappa B activation and MAPK pathway. Journal of Nutritional Biochemistry. 23(9):1184-1191.
Neville, M.C., Anderson, S.M., McManaman, J.L., Badger, T.M., Bunik, M., Contractor, N., Crume, T., Dabelea, D., Donovan, S.M., Forman, N., Frank, D.N., Friedman, J.E., German, J.B., Goldman, A., Hadsell, D., Hambidge, M., Hinde, K., Horseman, N.D., Hovey, R.C., Janoff, E., Drebs, N.F., Lebrilla, C.B., Leman, D.G., Maclean, P.S., Meier, P., Morrow, A.L., Neu, J., Nommsen-Rivers, L.A., Raiten, D.J., Rijnkels, M., Seewaldt, V., Shur, B.D., Vanhouten, J., Williamson, P. 2012. Lactation and neonatal nutrition: Defining and refining the critical questions. Journal of Mammary Gland Biology and Neoplasia. 17(2):167-188.
Alekel, D.L., Weaver, C.M., Ronis, M.J., Ward, W.E. 2013. Nutritional influences on bone health and overview of methods. In: Watson, R.R., Preedy, V.R., editors. Bioactive Foods as Dietary Interventions for the Aging Population. Elsevier Ltd., Oxford, U.K. p. 357-370.
Ronis, M.J.J. 2013. Molecular mechanisms underlying the actions of dietary factors on the skeleton. In: Watson, R.R., Preedy, V.R., editors. Bioactive Foods as Dietary Interventions of the Aging Population. Elsevier Ltd., U.K. p. 421-432.
Ronis, M.J., Shankar, K., Badger, T.M. 2013. The toxic effects of calories. In: Klaaseen, C., editor. Casarett & Doull's Toxicology, Chapter 27, 8th Edition. New York, NY: McGraw-Hill. p. 1169-1186.
Ronis, M.J., Ward, W.E., Weaver, C.M. 2013. Skeletal effects of plant products other than soy. In: Watson, R.R., Preedy, V.R., editors. Bioactive Foods in Bioactive Food as Dietary Interventions for the Agiing Population. Elsevier Ltd., Oxford, U.K. p. 409-419.
Saben, J., Zhong, Y., Gomez-Acevedo, H., Thakali, K.M., Borengasser, S.J., Andres, A., Shankar, K. 2013. Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: Role in maternal obesity. American Journal of Physiology - Endocrinology and Metabolism. 305(1):E1-E14.
Ronis, M.J., Baumgardner, J.N., Sharma, N., Badeaux, J., Ferguson, M.E., Tong, Y., Wu, X., Cleves, M.A., Badger, T.M. 2013. Medium chain triglycerides dose-dependently prevent liver pathology in a rat model of non-alcoholic fatty liver disease. Experimental Biology and Medicine. 238(2):151-162.
Andres, A., Casey, P., Cleves, M., Badger, T.M. 2013. Body fat and bone mineral content of infants fed breast-milk, cow's-milk formula, or soy formula during the first year of life. Journal of Pediatrics. 163(1):49-54.
Montales, M.E., Rahal, O.M., Nakatani, H., Matsuda, T., Simmen, R.C. 2013. Repression of mammary adipogenesis by genistein limits mammosphere formation of human MCF-7 cells. Journal of Endocrinology. 218(1):135-149.
Andres, A., Bellando, J., Casey, P., Cleves, M., Badger, T.M. 2013. Effects of fat mass on motor development during the first two years of life. Infant, Child and Adolecscent Nutrition. 5(4):248-254.
Pabona, J.M., Dave, B., Su, Y., Montales, T.M., Delumen, B.O., Mejia, E., Rahal, O., Simmen, R.C. 2012. The soybean peptide lunasin promotes apoptosis of mammary epithelial cells via induction of tumor suppressor PTEN: similarities and distinct actions from soy isoflavone genistein. Genes and Nutrition. 8(1):79-80.
Ronis, M.J., Shankar, K., Gomez-Acevedo, H., Hennings, L., Singhal, R., Blackburn, M., Badger, T.M. 2012. Mammary gland morphology and gene expression differ in female rats treated with 17 beta-estradiol or fed soy protein isolate. Endocrinology. 153(12):6021-6032.