Robert Koza

Education

• North Adams State College, North Adams, MA, BS 1984 Biology
• University of New Hampshire, Durham, NH, MS 1986 Biochemistry
• University of New Hampshire, Durham, NH, PHD 1989 Biochemistry

Research Interests

• Aging
• Cardiovascular
• Genomics
• Metabolism
• Molecular and Cellular Biology

Biography

Dr. Koza leads the Epigenetics and Obesity Laboratory at MaineHealth Institute for Research and has served as a Faculty Scientist for >10 years. His research interests include non-genetic based molecular pathways of obesity and metabolic disease, and thermogenic mechanisms of energy expenditure that could provide a therapeutic target for preventing obesity and diabetes. Dr. Koza received a BA from North Adams State College and a PhD from the University of New Hampshire. His postdoctoral training was performed at the Wistar Institute in Philadelphia, PA and the Lankenau Medical Research Center in Wynnewood, PA. After his postdoctoral work, he was a Research Associate at The Jackson Laboratory in Bar Harbor, ME from 1994-1998 and an Instructor/Assistant Professor at the Pennington Biomedical Research Center (PBRC) in Baton Rouge, LA from 1998-2013. Dr. Koza has served on numerous NIH grant review panels (NIDDK and NIEHS), NIH training grant panels, and has reviewed grant applications for the DOD and NSERC (Canada). He is currently the Director of the MMCRI Summer Student Research Program and Chair of the MMC Scientific Review Committee.

Multifactorial Regulation of Metabolic Disease

Complex metabolic syndromes such as obesity are caused by interactions between an individual’s genetic predisposition and the nutritional and physical environment. The focus of our laboratory is to explore novel mechanisms that modulate metabolism and obesity.  Studies characterizing the physiological consequences of perturbed metabolic states caused by either genetic predisposition and/or targeted mutations in mice have identified pathways involved in lipid accumulation in adipocytes and energy expenditure.

During our studies to understand how epigenetic changes in the genome may contribute to the development of obesity and metabolic disease, we identified an imprinted gene, mesoderm specific transcript (MEST), which facilitates lipid storage in mice fed an obesogenic diet. MEST shows large inter-individual differences of expression in adipose tissue within a population of genetically identical mice that is predictive to future susceptibility to development of obesity.

Another goal of our studies is to identify mechanisms of energy expenditure associated with heat production that could be used to reduce obesity and improve overall metabolism. While numerous studies by our laboratory and others have investigated mitochondrial uncoupling protein 1 (UCP1) in this process, we are currently characterizing an alternative UCP1-independent thermogenic mechanism in a mouse model deficient in UCP1 that likely requires greater caloric energy for the production of heat. Once identified, this novel energy-expending mechanism may provide a novel therapeutic target to combat obesity and associated metabolic disease states such as diabetes and cardiovascular disease.

Selected Publications