Dr.RACHEL-PERRY | Society of Life Sciences (SoLS)

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EDITORIAL BOARD

Dr. RACHEL PERRY

Address 1	:
Address 2	:
Title	:	Dr.
First Name	:	RACHEL
Last Name	:	PERRY
University/Institution	:	Yale University
Phone #	:	203-506-5179
Email ID	:	[email protected]
City	:	New Haven
Country	:	United States
State	:	Connecticut
Zipcode	:	06510

Department	:	Internal Medicine/Endocrinology
Company Name	:


Brief Description of Research Interest :
Rachel Perry, Ph.D. is a Postdoctoral Fellow at the Yale University School of Medicine. Rachel earned her B.S. in Biomedical Engineering, her Ph.D. in Cellular & Molecular Physiology, and performed her postdoctoral training in Medicine/Endocrinology, all in the laboratory of Dr. Gerald Shulman. Her research interests include the mechanism(s) by which hyperinsulinemia and obesity drive tumor growth, the use of stable isotope tracer methods to measure tissue-specific metabolic flux rates, the ability of inflammation to alter insulin sensitivity and predispose to hepatocellular cancer, the ability of the microbiome to drive hyperinsulinemia, insulin resistance, and obesity, and the development of novel agents to intervene in insulin resistance, type 2 diabetes, NASH, and cancer. As Co-Director of Yale's Mouse Metabolic Phenotyping Center Physiology Core, Rachel assists investigators worldwide in performing clamp studies, glucose tolerance tests, and metabolic cage analysis to assess the metabolic phenotypes of their transgenic mice.
Representative Publications :
Perry RJ, Peng L,Abudukadier A, Kennedy L, Cline GW, Shulman GI (in press). Mechanism for leptin's acute insulin-independent effect to reverse diabetic ketoacidosis. J. Clin. Invest. Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL,Petersen KF, Kibbey RG, Goodman AL, Shulman GI (2016). Acetate mediates a gutbiome-brain-β cell axis to promote metabolic syndrome. Nature 534:213-7. Perry RJ, Borders CB, Cline GW, Zhang X-M,Alves TC, Petersen KF, Rothman DL, Kibbey RG, Shulman GI (2016). Propionate increases hepatic pyruvate cycling, anaplerosis and alters mitochondrial metabolism. J. Biol. Chem. 291:12161-70. Perry RJ, Zhang D, Zhang X-M, Boyer JL, ShulmanGI (2015). Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats. Science 347:1253-6. 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 (2015). Hepatic Acetyl CoA Links AdiposeTissue Inflammation to Hepatic Insulin Resistance and Type 2 Diabetes. Cell 160:745-58. Perry RJ, Lee S, Ma L, Zhang D, Schlessinger J,Shulman GI (2015). FGF1 and FGF19 reverse diabetes by suppression of the hypothalamic-pituitary-adrenal axis. Nature Communications 6:6980. Befroy DE, Perry RJ*, Jain N, Dufour S, Cline GW,Trimmer J, Brosnan J, Rothman DL, Petersen KF, Shulman GI (2014). Direct assessment of hepatic mitochondrial oxidative and anaplerotic fluxes in humans using dynamic ¹³C magnetic resonance spectroscopy. Nature Med. 20:98-102. Equal contributions. Perry RJ, Zhang X-M, Zhang D, Kumashiro N,Camporez J-P, Cline GW, Rothman DL, Shulman GI (2014). Leptin reverses diabetes by suppression of the hypothalamic-pituitary-adrenal axis. Nature Medicine 20:759-63. Perry RJ, Kim T, Zhang X-M, Lee H-Y, Pesta D,Popov VB, Zhang D, Rahimi Y, Jurczak MJ, Cline GW, Spiegel DA, Shulman GI(2013). Reversal of Hypertriglyceridemia, Fatty Liver Disease, and Insulin Resistance by a Liver-Targeted Mitochondrial Uncoupler. Cell Metab. 18:740-8.