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Dr. HamiltonMarc T. Hamilton, PhD

  • Associate Professor of Biomedical Sciences
  • Dalton Cardiovascular Research Center Investigator

Email: HamiltonM@missouri.edu

Research Interests: Functional genomics, exercise, lipid metabolism.

Teaching: Physiology

Multidisciplinary work exposes lab members to a diversity of modern research techniques, and experience with studies involving both animal and human tissues. Dr. Hamilton studies the molecular and physiological mechanisms by which physical inactivity causes chronic metabolic diseases related to poor plasma lipid metabolism (coronary artery disease, Type II diabetes, obesity). Studies have sought to discover the genes and signals linking physical inactivity to disease, especially those processes related to fatty acid metabolism in skeletal muscle.

Using microarray methodologies, our laboratory has been characterizing the response of a large percentage of the genome to exercise training, inactivity, and identifying both the transcriptional and post-transcriptional events influenced by fatty acids. Related research has been focused on our provocative finding that there is a large cluster of genes expressed in skeletal muscle that regulate plasma lipid metabolism. Skeletal muscle tissue may be an important site of synthesis for proteins that are secreted into the blood stream and then are important for protecting against metabolic diseases. Microarray work is also beginning to study human muscle during exercise, bedrest, and microgravity.

Our major emphasis has focused on the molecular mechanisms regulating skeletal muscle lipoprotein lipase (LPL). Using both physiological and molecular approaches, we are studying the specific cellular factors that so potently "turn-off" LPL activity in skeletal muscle capillaries by as much as 90% when young animals become sedentary or old animals age.

Related News:
More Standing, Less Sitting, Found to Promote 'Optimal Metabolism'

Selected Publications:
Hamilton M.T., D.G. Hamilton, T.W. Zderic. The Role of Low Energy Expenditure and Sitting on Obesity, Metabolic Syndrome, Type 2 Diabetes, and Cardiovascular Disease. Diabetes 56:2655-2667, 2007.

Zderic TW, Hamilton M.T. Physical Inactivity Amplifies the Sensitivity of Skeletal Muscle to the Lipid-Induced Downregulation of Lipoprotein Lipase Activity. J Appl Physiol. 2006 Jan:100(1):249-57

Hamilton, M.T., D.G. Hamilton, T.W. Zderic. Exercise physiology versus inactivity physiology: an essential concept for understanding lipoprotein lipase regulation. ESSR. 32(4): 161-166, 2004.

Bey, L, N. Akunuri, P. E. Hoffman, P. Zhao, D.G. Hamilton, and M.T. Hamilton. Patterns in global gene expression in rat skeletal muscle during unloading and low-intensity ambulatory activity. Physiological Genomics 13:157-167, 2003.

Bey, L. and M.T. Hamilton. A molecular reason to maintain daily low-intensity activity: Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity. J. Physiol. (London) 551.2: 673-682, 2003.


 
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Last Update: November 28, 2007