Medical College of Georgia

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Education & Training:

1991    BA University of Colorado

1995    PhD Northwestern University

1995-1997  Duke University (Postdoctoral)

Academic Positions:

1997-2002              Assistant Professor, Kent State University

2002-present   Associate Professor, Medical College of Georgia

Awards & Honors:

2005 Outstanding Young Faculty Award, Basic Sciences, School of Medicine

Research Funding:

National Institute of Arthritis, Musculoskeletal, and Skin Diseases (R01 AR049717-01A2)

“Effects of myostatin deficiency on bone strength” (ACTIVE, 2004-2008).
 

Research Goals:

The overall goal of our research is to elucidate the major factors that contribute to bone formation during growth, development, and aging in order to develop more effective preventative strategies for osteoporosis. Osteoporosis is a disease that results in approximately 1.5 million fractures per year and is caused by age-related bone loss; however, much of the variance in fracture risk is explained by the peak bone mass attained at skeletal maturity (approximately age 20). Understanding the factors that increase peak bone mass is therefore useful for preventing fractures later in life. We are primarily interested in muscle-bone interactions and the way(s) in which muscle mass increases bone mass through endocrine and mechanotransduction pathways. We use several mouse gene knockout models to understand relationships between bone metabolism and body composition including mice lacking myostatin (GDF-8), which have increased muscle mass and decreased fat mass, and mice lacking leptin, which have decreased muscle mass and increased fat mass.

APPROACHES:
We measure bone mass and density in mouse bones using micro-densitometry techniques such as dual energy x-ray absorptiometry (DEXA) and peripheral quantitative computed tomography (pQCT). We assess the material properties of bones (e.g., bone strength, stiffness, and brittleness) using mechanical testing. Serum markers of bone formation are studied using radioimmunoassay and fluorochrome labeling is used to identify forming bone surfaces in vivo.
Finally, we monitor the expression of osteogenic factors in bone using immunohistochemical techniques and gene microarray technology.
 

Publications:

2007 Hamrick M, Della-Fera MA, Hartzell D, Choi Y-H, Baile CA. Intrahypothalamic injections of leptin increase adipocyte apoptosis in peripheral fat pad and in bone marrow. Cell and Tissue Research 327: 133-141.

2006 Hamrick M.W., Pennington C, Webb N, Isales C. Resistance to body fat gain in double-muscled mice fed a high fat diet. International Journal of Obesity 30 (5): 868-870.

2006 Hamrick M, Samaddar T, Pennington C, McCormick J. Increased muscle mass with myostatin deficiency improves gains in bone strength with exercise. Journal of Bone & Mineral Research 21: 477-483.

2005 E. Montgomery, C. Pennington, C.M. Isales, M. Hamrick. Muscle-bone interactions in dystrophin-deficient and myostatin-deficient mice. Anatomical Record 286A: 814-822.

2005 Hamrick, M, Della-Fera MA, Choi Y-H, Pennington C, Hartzell D, Baile CA. Leptin treatment induces loss of bone marrow adipocytes & increases bone formation in leptin-deficient ob/ob mice. Journal of Bone & Mineral Research 20: 994-1001.
 

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Cellular Biology and Anatomy
School of Medicine  |  School of Graduate Studies
Please email comments, suggestions or questions to:
Nan Eaton, neaton@mcg.edu