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Valerie A. Galton, Ph.D.

Title(s):
Professor of Physiology

Department(s):
Physiology

Education:
U. London, BSC 1955
U. London, PHD 1958

Programs:
Program in Experimental and Molecular Medicine

Contact Information:

Dartmouth Medical School
HB 7700
Lebanon NH 03756
Office: Borwell 726W
Phone: 603-650-7735
Fax: 603-650-6130
Email: val.galton@dartmouth.edu


Selected Publications:

 

  • Galton VA, Wood ET, St Germain EA, Withrow CA, Aldrich G, St Germain GM, Clark AS, St Germain DL. Thyroid hormone homeostasis and action in the type 2 deiodinase-deficient rodent brain during development. Endocrinology. 2007 Jul;148(7):3080-8. Epub 2007 Mar 1. (view details on MedLine)

  • Hernandez A, Martinez ME, Liao XH, Van Sande J, Refetoff S, Galton VA, St Germain DL. Type 3 deiodinase deficiency results in functional abnormalities at multiple levels of the thyroid axis. Endocrinology. 2007 Dec;148(12):5680-7. Epub 2007 Sep 6. (view details on MedLine)

  • Schneider MJ, Fiering SN, Thai B, Wu SY, St Germain E, Parlow AF, St Germain DL, Galton VA. Targeted disruption of the type 1 selenodeiodinase gene (Dio1) results in marked changes in thyroid hormone economy in mice. Endocrinology. 2006 Jan;147(1):580-9. Epub 2005 Oct 13. (view details on MedLine)

  • Hernandez A, Martinez ME, Fiering S, Galton VA, St Germain D. Type 3 deiodinase is critical for the maturation and function of the thyroid axis. J Clin Invest. 2006 Feb;116(2):476-84. Epub 2006 Jan 12. (view details on MedLine)

  • Galton VA. The roles of the iodothyronine deiodinases in mammalian development. Thyroid. 2005 Aug;15(8):823-34. Review. (view details on MedLine)

  • St Germain DL, Hernandez A, Schneider MJ, Galton VA. Insights into the role of deiodinases from studies of genetically modified animals. Thyroid. 2005 Aug;15(8):905-16. Review. (view details on MedLine)

  • Ng L, Goodyear RJ, Woods CA, Schneider MJ, Diamond E, Richardson GP, Kelley MW, Germain DL, Galton VA, Forrest D. Hearing loss and retarded cochlear development in mice lacking type 2 iodothyronine deiodinase. Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3474-9. Epub 2004 Mar 1. (view details on MedLine)

  • Wasco EC, Martinez E, Grant KS, St Germain EA, St Germain DL, Galton VA. Determinants of iodothyronine deiodinase activities in rodent uterus. Endocrinology. 2003 Oct;144(10):4253-61. Epub 2003 Jul 10. (view details on MedLine)

  • Schneider MJ, Fiering SN, Pallud SE, Parlow AF, St Germain DL, Galton VA. Targeted disruption of the type 2 selenodeiodinase gene (DIO2) results in a phenotype of pituitary resistance to T4. Mol Endocrinol. 2001 Dec;15(12):2137-48. (view details on MedLine)

  • Galton VA, Martinez E, Hernandez A, St Germain EA, Bates JM, St Germain DL. The type 2 iodothyronine deiodinase is expressed in the rat uterus and induced during pregnancy. Endocrinology 142: 2123-2128, 2001. (view details on MedLine)


  • Professional Interests:

    The long-term goal of Dr. Galton's research is to elucidate the mechanisms of action of thyroid hormones at the molecular level through a study of the relationships among hormone metabolism, hormone receptor interactions and hormone action in both developing and adult mammals.

    Current studies are concerned with the critical roles played by the deiodinases, enzymes which either activate (D1 and D2) thyroxine (T4) by converting it to its metabolically more active derivative 3,5,3'-triiodothyronine (T3), or inactivate (D3) both T4 and T3 by converting them to inactive derivatives. After cloning the cDNAs for the D2 and D3 from Rana catesbeiana, Dr Galton’s group has shown that differential expression of these enzymes is essential for coordinated metamorphosis of the frog.


    The roles of D1, D2 and D3 in mammals in regulating thyroid function in general and during development in particular are now being assessed. The general hypothesis is that the D1 and the D2 provide for tissue specific adaptations of intracellular T3 production in response to endogenous or environmental threats to thyroid hormone homeostasis. This hypothesis is being tested using genetically altered mouse models that are deficient in one or more of the deiodinases. We have already created and initiated studies in a D2-deficient (D2KO) mouse. The D2KO mouse is fertile and the pups have no gross physiological or behavioral abnormalities. However, it exhibits a marked resistance to T4 at the level of the pituitary, and studies indicate that thermogenesis in their brown adipose tissue is compromised and that they are hearing impaired. The D1, the double D1/D2KO, the D3KO and the triple D1/D2/D3KO mouse models are now in hand and their phenotypes are currently being assessed. Studies in these various mouse models will greatly facilitate our understanding of the physiological roles of the three enzymes.

    Courses Taught:

    Medical Physiology 120 (Endocrine section)
    Physiology 115 Advanced Endocrine Physiology.
    PEMM 101 First year core course
    PEMM 271. Advanced Systems Biology

    Grant Information:

    5R0l HD0920-31 12/01/01-11/30/09 NIH/NICHD
    Principal Investigator: Valerie Anne Galton, Ph.D.
    "Mechanisms of thyroid hormone action in development."

    1RO1 HD060180-01A1 7/1/09-6/30/14 NIH/NICHD
    Principal Investigator: Valerie Anne Galton, Ph.D.
    "Pre-receptor Modulation of Thyroid Hormone Action in the Developing Brain."

    R01DK079946-01A1 08/01/08-07/31/13 NIH/NIDDK.
    Principal Investigator: D.L. St.Germain (PI) (VAG Co-investigator)
    "Impact of Nutrition and Illness on Thyroid Homeostasis."

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