Geza Bruckner, PhD's picture
Geza Bruckner, PhD

Room 209A Wethington Building

900 South Limestone Street

Lexington, Kentucky 40536-0200

Office Phone Number: 
(859) 218-0859
Fax Number: 
(859) 257-2454

Scholarly Interest

  • Lipid metabolism in feline hepatic lipidosis: Impact of taurine and carnitine
  • Lipid metabolism and cardiovascular function and disease (including trans fatty acids, omega 3 fatty acids, antioxidant status)
  • Dietary phtyoestrogen effects on sperm function and cardiovascular disease risk

Academic Appointments
• Professor Clinical Nutrition, University of Kentucky
• Professor Center for Toxicology, University of Kentucky
• Professor Nutritional Sciences, University of Kentucky

• University of Kentucky, Botany B.S.
• University of Kentucky, Animal Sciences Nutrition M.S.
• University of Kentucky, Nutrition & Toxicology Ph.D.
• Cornell University, Nutrition Postdoctorate

• Oswald Scholarship for Creative Research
• UK Faculty Enrichment Grant
• Gnotobiotic Association Research Awards, Vth International Symposium,
• Elected Kentucky Chapter Alpha Eta Allied Health Honorary Society
• Honorary Faculty of Science and Technology, University of Wolverhampton, England
• Kingston Award for Excellence in Teaching

Most of the work in Dr. Bruckner’s laboratory for the last 25 years has been focused on lipid metabolism and cardiovascular function and disease. Of particular interest has been the metabolism of trans fatty acids and omega 3 fatty acids. Of interest has been how these dietary fatty acids influence lipoprotein metabolism, platelet-endothelial cell interactions, microcirculatory blood flow and more recently the antioxidant status of the host. Other areas of research interest have been Gnotobiology (study of germfree animals), where the research has focused on the interactions of the gut microflora with fatty acid metabolism and subsequent alteration of bioactive lipids.

Current research has been aimed at: 1) defining the etiology of feline hepatic lipidosis. Feline hepatic lipidosis (FHL) is a well-recognized hepatopathy that is characterized by extensive lipid accumulation and diabetes mellitus and acute pancreatitis appear to contribute to the pathogenesis of FHL. Our findings show that a lack of n3 LPUFA in the diet during weight gain may predispose the feline to liver lipidosis, which is exacerbated by a weight reducing diet limited in n3 LPUFA. Based on the decreased number of mitochondria and peroxisomes, the primary mechanism involved in the pathogenesis appears to be decreased fatty acid oxidation; 2) elucidating the mechanisms by which phytoestrogens alter sperm function and reproductive capacity; 3) integration of complementary and alternative medicine (CAM) practices into the medical and health sciences curriculum and evaluating the acceptance of these practices by more traditional western health care professionals; and 4) reducing obesity and sedentary behaviors in highly structured environments and how alteration of these health risk factors may impact on worksite safety.

A list of Dr. Bruckner's publications is available by clicking here.