Ph.D. Physiology and Nutrition, University of Leeds, England, UK., 1994
M.S. with distinction, Physiology and Nutrition, University of Leeds, England, UK., 1992
B.S. Honors, Animal Science, University of Iasi, Romania

Postdoctoral Fellow, Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, WA, 1996-1998

Associate Professor of Physiology, Western University of Health Sciences, Basic Medical Sciences 2010-present

Associate Professor of Nutritional Neuroscience and Physiology, Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 2008-2009

Assistant Professor of Nutritional Neuroscience and Physiology, Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 2002-2008

Research Assistant Professor, College of Veterinary Medicine, Washington State University, Pullman, WA, 1998-2002

Invited Lecturer, University Pierre et Marie Curie, Paris, France, AgroParisTech, Paris, France, University of Suceava, Romania

Undergraduate:

Introductory Principles in Nutrition
Nutritional Aspects of Diseases
Neurobiology
First year seminar

Graduate:

Ingestive Behavior: factors controlling food intake and energy homeostasis
Physiology and Nutritional Neuroscience
Nutrient metabolism
Gastrointestinal Physiology
Endocrinology

Obesity and diabetes are major causes of morbidity and mortality worldwide Using a combination of molecular, neuroanatomical, behavioral, biochemical and physiological approaches we are investigating satiation signals that control eating and regulation of body weight. Consequently, we are interested in the reduction of sensitivity to satiation signals in response to dietary adaptation (particularly dietary fat) and subsequent development of hyperphagia and obesity. We have developed several research programs in the following areas: 1) the interaction between metabolic events, orosensory factors, and central functions relevant to the initiation and termination of eating and the development of long term feeding patterns; 2) the neural regulation of eating during obesity and development of type-2 diabetes; 3) the central and peripheral taste and motivational processes in obesity and diabetes; 4) the effects of chronic exposure to dietary fats on neural adaptation, subsequent overconsumption and weight gain; 5) the role of gut microbiota in intestinal chemosensation. The control of eating and regulation of body weight require integration of sensory neural processes originating in the oral cavity and viscera and those systems that assign actual hedonic value to a meal. In obesity, this intricate relationship is perturbed. Using rodent models of obesity and diabetes, my laboratory demonstrated that, similar to obese humans, obese rats have an increased avidity for palatable foods (sucrose and oils) that progresses during prediabetes and diabetes. We also showed, that animal prone to become obese exhibit a host of postoral behavioral and neural deficits and fail to integrate postabsorptive and orosensory effects of palatable tastants.

• Duca, F, Swartz, TD, Sakar, Y, Covasa, M. Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota. PLoS ONE 7(6):e39748, 2012.
• Duca, F, Swartz, TD, Sakar, Y, Covasa, M. Decreased intestinal nutrient response in diet-induced obese rats: role of gut peptides and nutrient receptors. International Journal of Obesity, 2012. doi:10.1038/ijo.2012.45.
• Swartz, TD, Duca, F, de Wouters, T, Sakar, Y, Covasa, M. Upregulation of intestinal T1R3 and SGLT-1 expression and increased sucrose intake in mice lacking gut microbiota. Br J Nutr 25, 1-10, 2011.
• Covasa M. Deficits in gastrointestinal responses controlling food intake and body weight. Am J Physiol Regul Integr Comp Physiol, 299:R423-439, 2010.
• Swartz TD, Savastano DM, Covasa M. Reduced sensitivity to cholecystokinin in male rats fed a high-fat diet is reversible. J Nutr. 140:1698-1703, 2010.
• Swartz TD, Duca F, Covasa M. Differential feeding behavior and vagal responses to CCK in obesity-prone and –resistant rats. Brain Res. 1308:79-86, 2010.
• Swartz TD, Hajnal A, Covasa M. Increased orosensory sensitivity to oils in CCK-1 receptor deficient rats. Physiol Behav. 99:109-117, 2010.
• Abraham H, Covasa M, Hajnal A. Cocaine- and amphetamine-regulated transcript (CART) peptide immunoreactivity in the brain of the CCK-1 receptor deficient obese OLETF rat. Experimental Brain Research 96(4):545-56, 2009
• Hajnal A, Margas WM, and Covasa M. Altered dopamine D2 receptor function and binding in obese OLETF rat. Brain Res. Bull 75: 70-76, 2008.
• Hajnal A, DeJonghe BC and Covasa M. Dopamine D2 receptors contribute to increased avidity for sucrose in obese OLETF rats lacking CCK-1 receptors. Journal of Neuroscience. 148:584-592, 2007.

For more articles click the following link: http://www.ncbi.nlm.nih.gov/pubmed?term=Covasa