My research focuses on understanding how obesity affects a part of the brain called the hypothalamus – the brain’s central regulator of food intake, metabolism, hormone release, and reproduction. Excess circulating nutrients in obese individuals cause dysfunction of the hypothalamic neurons that control food intake by interfering with normal protein folding in the endoplasmic reticulum (ER). When the protein folding load exceeds cellular capacity, an ER stress response is initiated by the cell via a defined set of signal transduction pathways. In hypothalamic food intake neurons, ER stress interferes with the ability of these cells to respond appropriately to hormonal signals and control appetite.
Obesity is becoming ever-more prevalent in the United States, and it is linked to a constellation of other disorders, including infertility. In mammals, reproductive function is regulated by hypothalamic gonadotropin-releasing hormone (GnRH), which controls pituitary gonadotropin release and subsequent gonadal function. Dysfunction of GnRH-producing neurons leads to infertility in both males and females. In my lab, we use ER stress-inducing chemicals to mimic obesity-induced ER stress in a cell culture model of GnRH neurons. Currently, my students and I are working to characterize ER stress-induced changes in gene expression in GnRH neurons and the signaling pathways that mediate these changes.
Outside of the lab & classroom, I enjoy cooking, trying local beers and wine, hiking, and Zumba. I also enjoy interacting with the Wabash community through attending theater, music, and athletic events.
Postdoctoral Fellowship, The Scripps Research Institute, Department of Metabolism & Aging
Ph.D. in Neuroscience, University of Virginia
B.S. in Neuroscience, Allegheny College
BIO 111 – General Biology I
BIO 212 – Cell Biology
BIO 315 – Organismal Physiology
BIO 371 – Special Topics: Molecular Endocrinology
BIO 401 – Senior Seminar
Kern A, Albarran-Zeckler R, Walsh HE, Smith RG. 2012. Apo-ghrelin receptor forms heteromers with DRD2 in hypothalamic neurons and is essential for anorexigenic effects of DRD2 agonism. Neuron, 73(2):317-32.
Walsh HE, Shupnik MA. 2009. Proteasome regulation of dynamic transcription factor occupancy on the GnRH-stimulated luteinizing hormone beta-subunit promoter. Molecular Endocrinology, 23(2):237-50.
Haisenleder DJ, Burger LL, Walsh HE, Stevens J, Aylor KW, Shupnik MA, Marshall JC. 2008. Pulsatile GnRH Stimulation of Gonadotropin Subunit Transcription in Rat Pituitaries: Evidence for the Involvement of Jun N-Terminal Kinase (JNK) but not p38. Endocrinology, 149(1):139-45.
Ferris HF, Walsh HE, Stevens J, Fallest PC, Shupnik MA. 2007. Luteinizing Hormone Beta Promoter Stimulation by cyclic AMP and Cooperation with GNRH1 in Transgenic Mice and LBetaT2 Cells. Biology of Reproduction, 77(6):1073-80.
Kowase T, Walsh HE, Darling DS, Shupnik MA. 2007. Estrogen Enhances GnRH-Stimulated Transcription of the LH Subunit Promoters via Altered Expression of Stimulatory and Suppressive Transcription Factors. Endocrinology, 148(12):6083-91.
Indiana Academy of Science Senior Research Grant, 2015
MAJORS & MINORS
- ASIAN STUDIES (MINOR)
- BUSINESS (MINOR)
- COMPUTER SCIENCE (MINOR)
- EDUCATION STUDIES (MINOR)
- ENGINEERING (DUAL-DEGREE)
- FINANCIAL ECONOMICS
- GENDER STUDIES (MINOR)
- Global Health (MINOR)
- HISPANIC STUDIES
- MODERN LANGUAGES
- MULTICULTURAL AMER. STUDIES (MINOR)
- Neuroscience (MINOR)
- PRE-MEDICINE (PRE-PROFESSIONAL)
- POLITICAL SCIENCE