Obesity/overweight is a major threat to the public health of the United States and has been acknowledged as the second leading cause of death, behind smoking. Obesity has been linked to diabetes, hypertension, cardiovascular disease, cancer, and a myriad of other health problems. Obesity is multifactorial, and is an end result of genetic, molecular, physiological, behavioral, and societal/environmental factors. Efforts to understand and manage this complex chronic disease have met with modest success. Obesity continues to grow in prevalence at an alarming rate in both adults and children. It is likely that research which transcends traditional boundaries of research and focuses on transdisciplinary, integrative approaches to research questions may provide the answers needed to conquer this critical threat to the health of individuals. This is the initial proposal for a competitive continuation of a research training program titled, """"""""Obesity: Genes to Man."""""""" The sponsoring institution is Pennington Biomedical Research Center, Louisiana State University System. The objective of this program is to train Ph.D. postdoctoral fellows to become productive research scientists capable of establishing scientific careers that further the efforts of the NIH to understand the complex interactions between genetic, molecular, physiological, and behavioral aspects of obesity. Many molecular biologists/geneticists have been attracted to the obesity research field but lack the physiological/metabolic/behavioral expertise to fully exploit their discoveries. Conversely, physiological/metabolic and behavioral studies need to be complemented by molecular and genetic approaches for a fuller understanding.
We aim to bride the divide between the molecular/genetic approaches and the physiological/behavioral studies by encouraging trainees to gain experience in multiple areas of obesity research. It is difficult to get such a wide oversight or expertise during predoctoral programs. Hence, it is important to provide opportunities at the postdoctoral level for training in complementary areas. Each trainee will be encouraged to develop these transdisciplinary research efforts to understand aspects of the obesity disease. The program will take advantage of the cutting-edge technologies and the wide range of research efforts related to obesity that are available at Pennington. This broad-based, integrative training program will enable trainees to write competitive grant proposals that will help them establish successful research careers in academia, academic medicine, governmental agencies, and in the private sector, as well as maintain an interdisciplinary infrastructure at Pennington. The scientists at Pennington are committed to postdoctoral research training and see this as inseparable from their goal of excellence in research.
|Henagan, Tara M; Laeger, Thomas; Navard, Alexandra M et al. (2016) Hepatic autophagy contributes to the metabolic response to dietary protein restriction. Metabolism 65:805-15|
|Gilmore, L Anne; Butte, Nancy F; Ravussin, Eric et al. (2016) Energy Intake and Energy Expenditure for Determining Excess Weight Gain in Pregnant Women. Obstet Gynecol 127:884-92|
|Vandanmagsar, Bolormaa; Warfel, Jaycob D; Wicks, Shawna E et al. (2016) Impaired Mitochondrial Fat Oxidation Induces FGF21 in Muscle. Cell Rep 15:1686-99|
|MÃ¼nzberg, Heike; Qualls-Creekmore, Emily; Yu, Sangho et al. (2016) Hedonics Act in Unison with the Homeostatic System to Unconsciously Control Body Weight. Front Nutr 3:6|
|Sutton, Elizabeth F; Gilmore, L Anne; Dunger, David B et al. (2016) Developmental programming: State-of-the-science and future directions-Summary from a Pennington Biomedical symposium. Obesity (Silver Spring) 24:1018-26|
|Henagan, Tara M; Stefanska, Barbara; Fang, Zhide et al. (2015) Sodium butyrate epigenetically modulates high-fat diet-induced skeletal muscle mitochondrial adaptation, obesity and insulin resistance through nucleosome positioning. Br J Pharmacol 172:2782-98|
|Wanders, Desiree; Burk, David H; Cortez, Cory C et al. (2015) UCP1 is an essential mediator of the effects of methionine restriction on energy balance but not insulin sensitivity. FASEB J 29:2603-15|
|Henagan, T M; Cefalu, W T; Ribnicky, D M et al. (2015) In vivo effects of dietary quercetin and quercetin-rich red onion extract on skeletal muscle mitochondria, metabolism, and insulin sensitivity. Genes Nutr 10:451|
|Gao, Zhanguo; Zhang, Jin; Henagan, Tara M et al. (2015) P65 inactivation in adipocytes and macrophages attenuates adipose inflammatory response in lean but not in obese mice. Am J Physiol Endocrinol Metab 308:E496-505|
|Laque, Amanda; Yu, Sangho; Qualls-Creekmore, Emily et al. (2015) Leptin modulates nutrient reward via inhibitory galanin action on orexin neurons. Mol Metab 4:706-17|
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