2800 Plymouth Rd., NCRC Bldg 20
Ann Arbor, MI 48109
Available to mentor
Dr. Myers received his undergraduate degree in Molecular Biology (summa cum laude) at Princeton University in 1988 and his M.D. and Ph.D. (Cell Biology) degrees from Harvard Medical School in 1997. He joined the faculty at the Joslin Diabetes Center at Harvard Medical School in 1997, where he began to focus his independent research laboratory on mechanisms of leptin receptor signaling and links to the regulation of mammalian physiology. In 2004, Dr. Myers moved to the University of Michigan as a Michigan Biomedical Sciences Scholar and joined the faculty of Internal Medicine and Molecular and Integrative Physiology. Dr. Myers is the Director of the Elizabeth Weiser Caswell Diabetes Institute and the Michigan Diabetes Research Center.
Dr. Myers has been recognized with numerous awards and accolades. He received the Michigan Biomedical Sciences Scholar Award in 2004, was elected to the ASCI in 2005, received the Jerome Conn Award for Excellence in Research in 2006, and the American Diabetes Association’s Outstanding Scientific Achievement Award in 2010.
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Postdoctoral FellowHarvard Medical School/Joslin Diabetes Center, Boston, 1997
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MDHarvard University, Cambridge, 1997
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PhDHarvard University, Cambridge, 1997
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ABPrinceton University, Princeton, 1988
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Center MemberCaswell Diabetes Institute
Dr. Myers’ research focuses on how the central nervous system controls processes that enable the body to control blood glucose and body weight, and how problems in these pathways contribute to the development of insulin resistance and diabetes. His laboratory focuses on the crucial roles played by nerve centers in the unconscious part of the brain — including regions that control food intake and metabolism to regulate body weight, and “glycemic control centers” that regulate the body’s ability to control blood sugar.
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Sáenz de Miera C, Bellefontaine N, Allen SJ, Myers MG, Elias CF. 2024 Jul 15;PreprintGlutamate neurotransmission from leptin receptor cells is required for typical puberty and reproductive function in female mice.
DOI:10.7554/eLife.93204 PMID: 39007235 -
Sáenz de Miera C, Bellefontaine N, Allen SJ, Myers MG, Elias CF. eLife, 2024 Jun 6;Journal ArticleGlutamate neurotransmission from leptin receptor cells is required for typical puberty and reproductive function in female mice
DOI:10.7554/elife.93204.2 -
Hashsham A, Kodur N, Su J, Tomlinson AJ, Yacawych WT, Flak JN, Lewis KT, Oles LR, Mori H, Bozadjieva-Kramer N, Turcu AF, MacDougald OA, Myers MG, Affinati AH. 2024 May 21;PreprintControl of Physiologic Glucose Homeostasis via the Hypothalamic Modulation of Gluconeogenic Substrate Availability.
DOI:10.1101/2024.05.20.594873 PMID: 38826340 -
Saenz de Miera Patin C, Bellefontaine N, Allen S, Myers M, Elias C. bioRxiv,Journal ArticleGlutamate neurotransmission from leptin receptor cells is required for typical puberty and reproductive function in female mice.
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de Miera CS, Bellefontaine N, Allen SJ, Myers MG, Elias CF. 2024 Feb 28;Journal ArticleGlutamate neurotransmission from leptin receptor cells is required for typical puberty and reproductive function in female mice
DOI:10.7554/elife.93204.1 -
Levine SR, Myers MG, Barunas R, Chang DS, Dutta S, Maddess T, Liebmann JM, Sherman S, Eydelman M, Sun JK, Chambers W, Wickström K, Luhmann UFO, Pallinat M, Glassman A, Aiello LP, Markel DS, Gardner TW. Transl Vis Sci Technol, 2023 Nov 1; 12 (11): 33Journal ArticleReport From the 2022 Mary Tyler Moore Vision Initiative Diabetic Retinal Disease Clinical Endpoints Workshop.
DOI:10.1167/tvst.12.11.33 PMID: 38015167 -
de Miera CS, Bellefontaine N, Allen SJ, Myers MG, Elias CF. 2024 Mar 22;PreprintGlutamate neurotransmission from leptin receptor cells is required for typical puberty and reproductive function in female mice.
DOI:10.1101/2023.09.21.558865 PMID: 37790549 -
Rupp AC, Tomlinson AJ, Affinati AH, Yacawych WT, Duensing AM, True C, Lindsley SR, Kirigiti MA, MacKenzie A, Polex-Wolf J, Li C, Knudsen LB, Seeley RJ, Olson DP, Kievit P, Myers MG. J Clin Invest, 2023 Oct 2; 133 (19):Journal ArticleSuppression of food intake by Glp1r/Lepr-coexpressing neurons prevents obesity in mouse models.
DOI:10.1172/JCI157515 PMID: 37581939