Regents' Professor

Dr. Ruth Harris

 Phone: (706) 721-4479
 Fax: (706) 721-7299
 Email: RUHARRIS@augusta.edu
 Office: CA-1018
 Lab: CA-1054A

 

 

 

Learn more about Dr. Harris' 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

2018-present - Regents' Professor, Department of Physiology and College of Graduate Studies, Augusta University

2009-2018 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 models. We use very low, threshold doses of leptin to demonstrate that responsive areas in both the forebrain and hindbrain have to be activated simultaneously in order for exogenous leptin to inhibit food intake and cause weight loss. Exogenous leptin replicates the conditions that would be present when body fat starts to increase in response to excess energy intake. A number of hypothalamic nuclei are activated in response to leptin, but the ventromedial nucleus of the hypothalamus contains a large number of leptin receptors and appears to be essential in the integrated response to leptin that is initiated as a corrective action in conditions of positive energy balance. Our current research is focused on identifying the neural pathway that facilitates the integrated response and also to determine how activation of the ventromedial hypothalamus interacts with short-term satiety signals to inhibit food intake.

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.


honors and awards

2017 Distinguished Research Award - Augusta University Research Institute
2012 Distinguished Faculty Award for Basic Science Teaching - Faculty Senate of the Medical College of Georgia

(Go to Pub Med)

Desai, B.N., Harris, R.B. 2015. Leptin in the hindbrain facilitates phosphorylation of STAT3 in the hypothalamus. Am J Physiol Endocrinol Metab 308: E351-361
Harris, R.B.S., Desai B.N. 2016 Fourth ventricle leptin infusions dose dependently activate hypothalamic signal transducer and activator of transcription 3 (STAT3). Am J Physiol Endocrinol Metab 311:E939-E948
Harris, R.B. 2019. Low dose infusions of leptin into the nucleus of the solitary tract increase sensitivity to third ventricle leptin. Am J Physiol Endocrinol Metab. 316:E719-E728.
Seamon, M., Ahn, WA., Li, AJ., Ritter, S. and Harris, R.B.S. 2019 Leptin receptor-expressing neurons in the ventromedial nucleus of the hypothalamus contribute to weight loss caused by fourth ventricle leptin infusions. Am J Physiol Endocrinol 317: E586-E596
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: R543-555
Harris R.B., 2018 Source of dietary sucrose influences development of leptin resistance in male and female rats Am J Physiol. Regul Integr Comp Physiol 314: R589-610
Harris, R.B. 2019. Development of leptin resistance in sucrose drinking rats is associated with consuming carbohydrate-containing solutions and not calorie-free sweet solution. Appetite 132: 114-121.