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Whitney W. Woodmansee, M.D., Associate Clinical Professor of Medicine

Dr. Woodmansee is a Colorado native.  She is board certified in Internal Medicine and Endocrinology.  After completing her fellowship in Endocrinology, Metabolism, and Diabetes, she joined the Division as an Assistant Professor in 2000. 

Dr. Woodmansee’s general research area is in the field of neuroendocrinology.  She performs both basic science and clinical research.  Her basic science research is in the area of pituitary regulation and tumorigenesis.  Specifically, she is interested in the role of the hormone somatostatin in regulation of the hypothalamic-pituitary-thyroid axis.  Her work has focused on somatostatin’s role in the inhibition of thyrotrope (TSH producing cell) proliferation and hormone secretion.  Much of her research is related to understanding regulation of the somatostatin receptor type 5 gene and its role in thyrotrope function.  She has been involved in determining the structure of this gene and its transcriptional regulation.  Somatostatin receptors also play a role in regulation of a variety of other neuroendocrine tumors.  Consequently, in addition to enhancing our understanding of the basic molecular mechanisms of the somatostatinergic system and pituitary regulation, this research may have long range clinical applications regarding the pathogenesis and treatment of neuroendocrine tumors.  Dr. Woodmansee’s clinical research focuses on thyroid disease.  She is interested in the clinical consequences associated with mild forms of thyroid hyper and hypofunction.  She currently directs a project designed to study the metabolic alterations associated with mild hyperthyroidism and hypothyroidism.

As a clinician, Dr. Woodmansee practices general endocrinology.  However, she specializes in all types of pituitary and thyroid disease.  She currently participates in a joint pituitary tumor clinic with neurosurgeon Dr. Kevin Lillehei

Selected Publications

  • Golden WM, Weber KB, Hernandez TL, Sherman SI, Woodmansee WW, Haugen BR. Single-dose rexinoid rapidly and specifically suppresses serum thyrotropin in normal subjects. J Clin Endocrinol Metab. 2007 PUBMED

  • Sarapura VD, Wood WM, Woodmansee WW, Haakinson DJ, Dowding JM, Gordon DF, Ridgway EC. Pituitary tumors arising from glycoprotein hormone alpha-subunit-deficient mice contain transcription factors and receptors present in thyrotropes. Pituitary. 2006;9(1):11-8 PUBMED

  • Sarapura VD, Wood WM, Woodmansee WW, Haakinson DJ, Dowding JM, Gordon DF, Ridgway EC. Pituitary tumors arising from glycoprotein hormone alpha-subunit-deficient mice contain transcription factors and receptors present in thyrotropes. Pituitary. 2006 PUBMED

  • Woodmansee WW, Kerr JM, Tucker EA, Mitchell JR, Haakinson DJ, Gordon DF, Ridgway EC, Wood WM. The proliferative status of thyrotropes is dependent on modulation of specific cell cycle regulators by thyroid hormone. Endocrinology. 2006 Jan;147(1):272-82. PUBMED

  • Kerr JM, Gordon DF, Woodmansee WW, Sarapura VD, Ridgway EC, Wood WM. Growth arrest of thyrotropic tumors by thyroid hormone is correlated with novel changes in Wnt-10A. Mol Cell Endocrinol. 2005 Jun 30;238(1-2):57-67. PUBMED

  • Woodmansee WW, Haugen BR. Uses for recombinant human TSH in patients with thyroid cancer and nodular goiter. Clin Endocrinol (Oxf). 2004 Aug;61(2):163-73. PUBMED

  • Gordon, D.F., Woodmansee, W.W., Black, J.N., Dowding, J.M., Bendrick-Peard, J., Wood, W.M., and Ridgway, E.C.  Domains of Pit-1 important for transcriptional synergy with GATA-2 on the mouse TSHb gene.  Molecular and Cellular Endocrinology, 196: 53-66. 2002. PUBMED