Professor

Dr. Ruth Harris

 Phone: (706) 721-4479
 Fax: (706) 721-7299
 Email: RUHARRIS@augusta.edu
 Office: CA-1020
 Lab: CB-1054A

 

 

 

LEARN MORE ABOUT DR. Harris's RESEARCH


Education and Training

University of Georgia
Postdoctoral fellowship, Foods and Nutrition
Laboratory of Roy Martin, 1981-1984

University of Leeds, England
PhD, 1981

University of Leeds, England
BSc Food Science and Physiology, 1977


Academic Appointments

2009-present - Professor, Department of Physiology and College of Graduate Studies, Augusta University

2005-2009 - Professor, Department of Foods and Nutrition, University of Georgia

2000-2005 - Associate Professor, Department of Foods and Nutrition, University of Georgia

1999-2000 - Associate Professor, Department of Neuroscience, Pennington Biomedical Research Center, Baton Rouge, LA

1994-1999 - Assistant Professor, Department of Neuroscience, Pennington Biomedical Research Center, Baton Rouge, LA

1987-1988 - Assistant Member, Monell Chemical Senses Center, Philadelphia, PA


Research Interests

I have a long-standing interest in the feedback regulation of energy balance and recently we have focused on the role of leptin in this system. Leptin is released by adipose tissue and acts as a feedback signal to regulate body fat content. We are focusing on how and where leptin is acting in the brain to modify food intake, energy expenditure and body fat. We also are interested in how diet-induced changes in metabolism cause leptin resistance.

The first of our current projects investigates how leptin activity in the hindbrain integrates with that in the forebrain to influence energy balance and body composition using rat and mouse models. We have determined that leptin responsive areas in both the forebrain and hindbrain have to be activated simultaneously in order for leptin to inhibit food intake and cause weight loss and are now investigating how these two areas of the brain communicate with one another to optimize leptin responsiveness.

A second research interest is to determine how changes in diet composition can modify leptin responsiveness.  We have found that rats given access to sucrose solution in addition to their regular diet rapidly develop leptin resistance without becoming obese.  It appears that consumption of simple carbohydrate may activate the hexosamine biosynthetic pathway.  The product of this pathway, UDPGlcNAc, is a substrate for O-GlcNAc modification of threonine and serine residues of proteins, including those involved in leptin signaling. We are testing the hypothesis that O-GlcNAc modification interferes with activation of the transcription factor signal transducer and activator of transcription 3 (STAT3), which is required for leptin to control energy balance.

*Representative Publications*

(Go to Pub Med)

Harris, R.B.S. 2013 Contribution made by parabiosis to the understanding of energy balance regulation. BBA-Molecular Basis of Disease (Review) 1832:1449-1455.

Harris, R.B.S. Direct and Indirect Effects of Leptin on Adipocyte Metabolism. 2013 BBA-Molecular Basis of Disease (Review) 1842:414-423.

Desai, B.N. and Harris, R.B.S. 2013. Integrated effects of leptin in the forebrain and hindbrain of male rats. Endocrinology 154: 2663-2675.

Harris, R.B.S. 2013. Evidence that leptin-induced weight loss requires activation of both forebrain and hindbrain receptors. Physiol Behav 120:83-92.

Desai, B.N., Harris, R.B. 2015. Leptin in the hindbrain facilitates phosphorylation of STAT3 in the hypothalamus. Am J Physiol Endocrinol Metab. 308:E351-61.

Vasselli, J.R., Scarpace, P.J., Harris R.B.S., and Banks, W.A. 2013. Dietary components in the development of leptin resistance. Advan Nutr 4: 164-175.

Zimmerman, A.D., Harris, R.B.S. 2015.  In vivo and vitro evidence that chronic activation of the hexosamine biosynthetic pathway interferes with leptin-dependent STAT3 phosphorylation. Am J Physiol Reg Integr Comp 308:R543-55.

Harris, R.B.S., Apolzan,J.W. 2015.   Hexosamine biosynthetic pathway activity in leptin resistant sucrose-drinking rats. Physiol Behav 138:208-218.