David Clemmons, MD

David Clemmons, MD

Office: 919-966-0134
Appts: 984-974-2950
Curriculum Vitae

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Sarah Graham Kenan Professor of Medicine

Specialty Areas: Consultative endocrinology; pituitary and adrenal disease; growth hormone; insulin-like growth factor-I

ChronologyMD: University of North Carolina, 1974; Intern and Resident: Massachusetts General Hospital, Boston, MA, 1974-1976; Resident: Johns Hopkins, Baltimore, MD, 1976-1977; Fellowship Endocrinology: Massachusetts General Hospital, Boston, MA, 1977-1979; Assistant Professor of Medicine: University of North Carolina, 1979-1985; Associate Professor of Medicine: University of North Carolina, 1985-1990; Professor of Medicine: University of North Carolina, 1990-1995; Kenan Professor of Medicine: University of North Carolina, 1996-present.

Dr. Clemmons combines basic biomedical research, clinical investigation and consultative endocrinology practice as well as clinical education. His basic research involves understanding the molecular mechanisms by which insulin-like growth factors stimulate cellular proliferation and differentiation. Dr. Clemmons is also interested in how cells that are undergoing hyperglycemic stress respond aberrantly to stimulation by these growth factors. Additionally he is interested in the mechanisms by which these factors stimulate differentiation particularly in osteoblasts and vascular cells. His clinical studies involve novel methods for reversing the effect of these factors in patients with diabetic nephropathy and retinopathy. In his clinical practice he combines his interest in growth hormone and IGF-I with the assessment of patients with hypopituitarism and patients with pituitary tumors that hypersecrete growth hormone or prolactin.

Selected Bibliography:

Maile LA, Busby WH Jr, Nichols TC, Bellinger DA, Merricks EP, Rowland M, Veluvolu V, Clemmons DR. A monoclonal antibody against the αVβ3 integrin inhibits development of atherosclerotic lesions in diabetic pigs. Sci Trans Med 2:62-69, 2010. 

Xi G, Shen XC, Wai C, Clemmons DR. Recruitment of Nox4 to a plasma membrane scaffold is required for localized ROS generation and sustained Src activation in response to IGF-I. J Biol Chem. 288(22):15641-53, 2013. 

Xi G, Shen X, Rosen CJ, Clemmons DR.IRS-1 functions as a molecular scaffold to coordinate IGF-I/ IGFBP-2 signaling during osteoblast differentiation. J Bone and Miner Res. 31:1300-1314, 2016.