Obesity/overweight is rampant in the U.S. and has been acknowledged as the second leading cause of death. Obesity has been linked to diabetes, hypertension, cardiovascular disease, and cancer. Efforts to understand and manage this complex disease have met with modest success such that 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 cross-disciplinary approaches to research questions may provide the answers needed to conquer this grave threat to the health. This application is a request for renewal funding for the Pennington Biomedical Research Center (Louisiana State University System) training program """"""""Obesity: From Genes to Man"""""""". This program was funded originally in 2003, and renewed successfully in 2007. One of the aims of this grant is to train postdoctoral fellows in the complex interactions between genetic, molecular, physiological, and behavioral aspects of obesity. The objective of this program is to train Ph.D. and M.D. postdoctoral fellows to become productive research scientists capable of establishing scientific careers in academia, academic medicine, governmental agencies, and in the private sector. These junior scientists will further the efforts of the NIH to understand the complex interactions between genetic, molecular, physiological, and behavioral aspects of obesity. Many molecular biologists/geneticists are interested in obesity-related research, but lack the physiological/metabolic/behavioral expertise to maximize their research discoveries. Conversely, physiological /metabolic/behavioral studies need molecular and genetic approaches for a fuller understanding.
We aim to bridge the divide between the molecular/genetic approaches and the physiological/behavioral studies of the functions of specific genes by providing training in these areas. Each postdoctoral fellow will be encouraged to develop these transdisciplinary research efforts to understand multiple aspects of obesity and obesity-related disease. The program will take advantage of the cutting-edge technologies and the wide range of research efforts related to obesity available at Pennington Biomedical. This broad-based, training program will enable trainees to acquire transdisciplinary research skills and write competitive grant proposals addressing important questions which will move our science forward. The faculty of Pennington Biomedical are committed to postdoctoral research training and see this as inseparable from their goal of excellence in research. This application is requesting five additional years of funding for six (6) trainee positions per year. We will recruit M.D.s and Ph.D.s from the basic, clinical, and population science disciplines including biology, physiology, kinesiology, neuroscience, public health, and psychology. The majority of trainees will enter into the program with no prior postdoctoral training. However, for the first year of funding, we have requested three slots for individuals with prior training in order to accommodate those fellows currently in the program who remain eligible to continue. Trainees will be supported for two to three years.

Public Health Relevance

Obesity/overweight is the second leading cause of death, and has been linked to diabetes, high blood pressure, and cancer. Research which focuses on combining approaches from basic, clinical, and population science may find the answers needed to conquer this public health threat. The objective of this grant is to train junior-level scientists in understanding the complex relationships between genetic, molecular, physiological, behavioral, and population aspects of obesity.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Institutional National Research Service Award (T32)
Project #
Application #
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Densmore, Christine L
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Lsu Pennington Biomedical Research Center
Organized Research Units
Baton Rouge
United States
Zip Code
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
Münzberg, 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

Showing the most recent 10 out of 64 publications