Matthew Potthoff, PhD

Contact Information

Office: 3322 PBDB 
Phone: 319-384-4438 
Faculty Profile

Brief description of current research:

Obesity and insulin resistance are major contributors to the epidemic of metabolic diseases including dyslipidemia, hypertension and type 2 diabetes. My research is focused on the physiological mechanisms that regulate metabolic homeostasis and insulin sensitivity. We are specifically interested in unraveling hepatic pathways that govern systemic energy balance and glucose homeostasis in hopes of identifying a new therapeutic to treat obesity and metabolic disease. This has led me to study the diverse functions of the endocrine hormone fibroblast growth factor 21 (FGF21) which is produced in the liver during nutritional deprivation and surfeit. Utilizing novel transgenic mouse models, classical pharmacological methodologies, and state-of-the-art tracer techniques we have uncovered novel mechanisms regulating insulin sensitivity that could lead to new treatments for cardiovascular and metabolic disease.

3 most influential diabetes/obesity/metabolism publications:

  • Potthoff, M.J., Potts, A., He, T., Duarte, J.A., Taussig, R., Mangelsdorf, D.J., Kliewer, S.A., Burgess, S.C.: Colesevelam Suppresses Hepatic Glycogenolysis by TGR5-mediated Induction of GLP-1 Action in DIO Mice. American Journal of Physiology: Gastrointestinal and Liver Physiology, 304(4):G371-G380, 2013. PMCID: PMC3566618 [Available on 2014/2/15]
  • Potthoff, M.J., Boney-Montoya, J., Choi, M., Satapati, S., He, T., Suino-Powell, K., Xu, H.E., Gerard, R.D., Finck, B.N., Burgess, S.C., Mangelsdorf, D.J., Kliewer, S.A.: FGF15/19 Regulates Hepatic Glucose Metabolism By Inhibiting the CREB-PGC-1a Pathway. Cell Metab. 13(6):729-738, 2011. PMCID: PMC3131185.
  • Potthoff, M.J., Inagaki, T., Satapati, S., Ding, X., He, T., Goetz, R., Mohammadi, M., Finck, B.N., Mangelsdorf, D.J., Kliewer, S.A., Burgess, S.C.: FGF21 induces PGC-1a and regulates carbohydrate and fatty acid metabolism during the adaptive starvation response. PNAS. 106(26):10853-10858, 2009. PMCID: PMC2705613