Rachel Perry

2016 Regional Award Finalist — Post-Doc

Rachel Perry

Current Position:
Postdoctoral Fellow

Yale University

Biomedical Engineering & Biotechnology

Recognized for: Developing methodologies and uncovering mechanisms driving insulin resistance in animal models of diabetes

Areas of Research Interest and Expertise:  In vivo physiology, metabolism, tracer methodology

Rachel Perry


PhD, Cellular & Molecular Physiology, Yale University 
BS, Biomedical Engineering, Yale University 

Dr. Perry is an expert in the use of tracer methodology to model in vivo physiology.  She developed a novel NMR/LC-MS/MS flux method to model all key liver-specific oxidative and anaplerotic flux rates in awake rodents. Dr. Perry’s studies have generated key observations explaining the pathogenesis of diabetic ketoacidosis and the ability of insulin to suppress gluconeogenesis in rodents and humans, linking both phenomena to alterations in lipolysis and hepatic acetyl CoA content. She applied this method to demonstrate the mechanisms of action of two novel mitochondrial uncoupling agents which she found burned liver fat and resolved both type 2 diabetes and non-alcoholic steatohepatitis in rodents.

Dr. Perry’s recent work has focused on identification of a mechanism by which the gut microbiota drive the metabolic syndrome in rodents by increasing acetate turnover, parasympathetic activity, hyperinsulinemia, hyperphagia, and obesity. She is embarking on a project seeking to understand how changes in oxidative fluxes in tumors may explain the effect of insulin resistance and hyperinsulinemia to promote tumor growth in certain cancers.

Dr. Perry’s long-term goal is to direct a laboratory investigating the role of changes in glycolytic and oxidative flux rates due to hyperinsulinemia and/or inflammation in driving tumor pathogenesis.

“The goal of my research is to develop state-of-the-art methods to measure rates of metabolic pathways in liver that are dysregulated in diabetes. Using these methods, we aim to uncover new insights into the pathogenesis of, and potential treatments for, the epidemics of obesity and diabetes and their associated conditions, including cardiovascular disease, stroke, and cancer.”

Key Publications: 

  1. Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL, Petersen KF, Kibbey RG, Goodman AL, Shulman GI. Acetate mediates a gut biome-brain-β cell axis to promote metabolic syndrome. Nature. 2016
  2. Perry RJ, Camporez JP, Kursawe R, Titchenell PM, Zhang D, Perry CJ, Jurczak MJ, Abudukadier A, Han MS, Zhang X-M, Ruan H-B, Yang X, Caprio S, Kaech SM, Sul HS, Birnbaum MJ, Davis RJ, Cline GW, Petersen KF, Shulman GI. Hepatic Acetyl CoA Links Adipose Tissue Inflammation to Hepatic Insulin Resistance and Type 2 Diabetes. Cell. 2015
  3. Perry RJ, Zhang D, Zhang X-M, Boyer JL, Shulman GI. Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats. Science. 2015
  4. Perry RJ, Zhang X-M, Zhang D, Kumashiro N, Camporez J-P, Cline GW, Rothman DL, Shulman GI. Leptin reverses diabetes by suppression of the hypothalamic-pituitary-adrenal axis. Nature Medicine. 2014