Penn State Harrisburg
Middletown, PA 17057
Biography
Dr. David Williamson’s research seeks to delineate mechanisms that regulate aberrant growth signaling that contribute to skeletal muscle anabolic resistance in type 2 diabetes, obesity, and aging. Given his graduate training in human muscle physiology at the Human Performance Laboratory at Ball State, he expanded my knowledge of muscle physiology during his post-doctoral training at Hershey Medical Center by employing animal and cell models. In doing so, he studied how AMPK activation alters mTOR and mRNA translation in physiological contexts. Then arriving at West Virginia University, he further sought to determine how altered states of AMPK and/or mTOR activation would influence muscle differentiation and/or growth, using cell and mouse models of obesity and aging. Then at the University at Buffalo his laboratory focused on aberrant regulation of mTOR during aging and obesity, establishing the role of the mTOR inhibitor, REDD1, on the development of an anabolic resistant skeletal muscle phenotype. This research is currently being supported by the National Institutes of Health (NIH)- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) for 5 years (DK119961). This mechanism may contribute to skeletal muscle cachexia in numerous models, such as type 2 diabetes, obesity, aging, cancer, and muscular dystrophy.
Research Interests
- Mechanisms of skeletal muscle anabolic resistance
- Interventions that improve insulin sensitivity
- Mechanisms of exercise-induced insulin sensitivity
Publications
Steiner JL, Johnson BR, Hickner RC, Ormsbee MJ, Williamson DL, Gordon BS. Adrenal stress hormone action in skeletal muscle during exercise training: An old dog with new tricks? Acta Physiol (Oxf). 2020 Jun 7;e13522. doi: 10.1111/apha.13522. Online ahead of print.
Dungan C.M., Gordon, B.S., and Williamson D.L. Acute treadmill exercise discriminately improves the skeletal muscle insulin-stimulated growth signaling responses in mice lacking REDD1. Physiol. Reports. e14011, 2019.
Gordon B.S., Steiner J.L., Rossetti M.L., Qiao S., Ellisen L.W., Govindarajan S.S., Eroshkin A.M., Williamson D.L., and Coen P.M. REDD1 Induction Regulates the Skeletal Muscle Gene Expression Signature following Acute Aerobic Exercise. Am. J. Physiol: Endo. Metab. 313:E737-E747, 2017.
Dungan C.M. and Williamson D.L. Regulation of skeletal muscle insulin-stimulated signaling through the MEK-REDD1-mTOR axis. Biochem. Biophys. Res. Comm. 482(4):1067-1072, 2017.
Williamson D.L. and Rideout, T.C. Is ACSL6 at the crossroads of lipid synthesis? Journal of Physiology, Perspective. 595(3):619-620, 2017.
Dungan C.M., Li, J., Williamson, D.L. Caloric Restriction Normalizes Obesity-Induced Alterations on Regulators of Skeletal Muscle Growth Signaling. Lipids. 51(8):905-912, 2016.
Gordon, B.S., Steiner, J.L., Williamson, D.L, Lang, C.H., Kimball, S.R. Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism. Am. J. Physiol: Endo. Metab. 311(1):E157-174, 2016.
Dungan C.M., Z. Li, D.C. Wright, D.L. Williamson. Hyperactive mTORC1 signaling is unaffected by metformin treatment in aged skeletal muscle. Muscle and Nerve, 53(1):107-17, 2016.
Williamson, D.L, Mahmoud, A.M., Mey, J.T., Blackburn, B.K., Haus, J.M. Aberrant REDD1-mTORC1 responses to insulin in skeletal muscle from type 2 diabetics. Am. J. Physiol: Regul Integr Comp Physiol. 309(8):R855-863, 2015.
Gordon, B.S., D.L. Williamson, C.H. Lang, L.S. Jefferson, S.R. Kimball. Nutrient-induced stimulation of protein synthesis in mouse skeletal muscle is limited by the mTORC1 repressor REDD1. J. Nutr. 145(4):708-713, 2015.
Li Z., C.M. Dungan, B. Carrier, T.C. Rideout, D.L. Williamson. Alpha-lipoic acid supplementation reduces mTORC1 signaling in skeletal muscle from high fat fed, obese Zucker rats. Lipids. 49(12):1193-201, 2014.
Mennes, E. C.M. Dungan, S. Frendo-Cumbo, D.L. Williamson, D.C. Wright. Aging-Associated Reductions in Lipolytic and Mitochondrial Proteins in Mouse Adipose Tissue Are Not Rescued by Metformin Treatment. J. Geront. A. Biol. Med. Sci. 69(9):1060-068, 2014.
Dungan C.M., D.C. Wright, D.L. Williamson. Lack of REDD1 reduces whole body glucose and insulin tolerance, and impairs skeletal muscle insulin signaling. Biochem. Biophys. Res. Comm. 453(4):778-783, 2014.
Williamson DL, Z. Li, R.M. Tuder, E. Feinstein, S.R. Kimball, C.M. Dungan. Altered nutrient response of mTORC1 as a result of changes in REDD1 expression: Effect of obesity versus REDD1 deficiency. J. Appl. Physiol. 117(3):246-256, 2014.
Wen S., Jadhav K.S., Williamson, D.L., and Rideout, T.C. Treadmill Exercise Training Modulates Hepatic Cholesterol Metabolism and Circulating PCSK9 Concentration in High-Fat-Fed Mice. Journal of Lipids, vol. 2013, Article ID 908048. (doi:10.1155/2013/908048).
Drake, J.C., S.E. Alway, J.M. Hollander, D.L. Williamson. AICAR treatment for 14 days normalizes obesity-induced dysregulation of TORC1 signaling and translational capacity in fasted skeletal muscle. Am. J. Physiol. 299:R1546-1554, 2010.
Education
Post-doctoral Training in Cell and Molecular Physiology Department (Pennsylvania State University, College of Medicine)
M.S.; Ph.D. (Ball State University)
B.S. (Pennsylvania State University)