Rachel 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. Rachel's CV includes first-author papers in Nature, Cell (2), Science, JCI, PNAS, Nature Medicine (2), PNAS, Nature Communications (3), JBC, Cell Metabolism (2), and AJP-Endocrinology.

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 (Wang et al. Cell Reports 2018, Nasiri et al. Cancer & Metabolism 2019), and went on to show that responsiveness to insulin is a metabolic signature of obesity-associated tumor types in vitro (Rabin-Court et al. PLoS One 2019).

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? (Close collaboration with Dr. Andrew Wang's lab.)