Rachel Jamison Perry, PhD

Dr. Rachel Perry is an Assistant Professor in Medicine/Endocrinology and Cellular & Molecular Physiology at the Yale University School of Medicine. Rachel's background is in the use of hyperinsulinemic-euglycemic clamps and stable isotope infusions to assess insulin sensitivity, having earned her B.S. in Biomedical Engineering, Ph.D. (with Distinction) in Cellular & Molecular Physiology, and performed her postdoctoral training in Medicine/Endocrinology, all in the laboratory of Dr. Gerald Shulman. She opened her independent laboratory with K99/R00 funding in 2018.

The Perry laboratory focuses on applying stable isotope tracer methods to understand obesity- and insulin-associated alterations in metabolic flux pathways. Dr. Perry and her colleagues have recently identified hyperinsulinemia-induced increases in tumor glucose uptake and oxidation as a critical driver of colon cancer in two mouse models of the disease, and mitochondrial uncoupling as a potential therapeutic strategy against the disease, and went on to show that responsiveness to insulin is a metabolic signature of obesity-associated tumor types in vitro. Current work in the Perry lab expands upon these themes to study the intersection between systemic metabolism and immunometabolism in cancer as well as in sepsis and exercise. We are currently funded by the NIH (R37, R21), the Melanoma Research Alliance, and the Juvenile Diabetes Research Foundation.

Current projects in the Perry lab include:

1. What is the molecular mechanism by which obesity and hyperinsulinemia promote tumor growth? How does insulin alter rates of glycolytic, oxidative, and anaplerotic metabolism? Can we invent better tracer methods than currently exist, allowing us to reliably measure rates of these pathways in vivo?

2. What is the impact of exercise, a classic insulin-sensitizing intervention, on obesity-associated tumor growth - and what is the mechanism?

3. Are alterations in tumor immunometabolism permissive for tumor progression? How does cancer therapy alter substrate preference in immune cells? Can we exploit systemic metabolic changes to enhance anti-cancer immunity?

4. How do tumor metabolism and immunometabolism differ - in rate and regulation - in metastases as compared to primary tumor?

5. What drives the changes in glucose metabolism commonly observed in inflammation that occurs following various stimuli?

In addition, Dr. Perry places great value on mentorship and has completed multiple trainings to help her hone these skills. The Perry lab is honored to have trainees at the high school, undergraduate, and graduate level from around the world working with us both remotely and in person.