Sarah Oppelt

Sarah Oppelt is an Assistant Professor at Central Washington University, based in the Science Building (Room 236K). She teaches undergraduate courses including Genetics, Advanced Cell Biology, and Techniques in Biotechnology Research, with research focused on metabolic pathways influencing cell fate decisions, particularly how dyslipidemia induces tissue metabolic distress, macrophage recruitment, and pro-inflammatory activation.

Her academic credentials include:

• Ph.D. in Molecular, Cell Biology, and Biochemistry, Boston University, 2016
• B.A. in Biology, Hartwick College, 2004

Dr. Oppelt's research spans Metabolism, Cell Biology, Dyslipidemia, Inflammation, Macrophage Biology, Atherosclerosis, and Fructose Metabolism. She investigates molecular mechanisms linking metabolic disturbances to inflammatory responses, with emphasis on tissue microenvironment alterations in metabolic diseases. Current projects explore dyslipidemia-driven macrophage activation pathways relevant to atherosclerosis and metabolic syndrome.

Analysis of her 2009-2018 publications reveals consistent focus on fructose metabolism's role in brain function, atherosclerosis development, and genetic metabolic disorders. Key themes include fructose-induced vasopressin secretion in dehydration, early plaque dynamics in atherosclerosis, and mouse models of hereditary fructose intolerance, demonstrating interdisciplinary approaches bridging neuroscience, endocrinology, and cardiovascular biology.

No scientific awards are documented in the provided materials.

Dr. Oppelt actively recruits Master's students and undergraduates for dyslipidemia and macrophage research projects. No specific grant funding or formal advising relationships are detailed in the available information.

She leads a research group examining metabolic-inflammation crosstalk, particularly how dyslipidemia alters tissue microenvironments to promote macrophage-driven inflammation, with implications for therapeutic interventions in cardiovascular and metabolic diseases.