Karin Bornfeldt

Abstract

Karin Bornfeldt is stubborn. Once she gets curious about something, she does not let it go—turning questions around in her head, examining the issue from varying perspectives, thinking about alternative solutions, and applying a variety of tools to the problem. The question that sparked Bornfeldt’s curiosity during her PhD research at the University of Linkoping was how diabetes mellitus accelerates atherosclerosis. She has never lost interest, and in 3 decades of research, she has worked to uncomplicate the most deadly of diabetic complications. Bornfeldt, joint professor of medicine and pathology at the University of Washington in Seattle, arrived at the university in 1991 as a postdoc to work with Russell Ross, PhD, and Edwin Krebs, MD. She joined the faculty in 1995 and is now associate director of the Diabetes and Obesity Center of Excellence, deputy director of the Diabetes Research Center, and director of the Viral Vector and Transgenic Mouse Core at the university. Karin Bornfeldt When Bornfeldt established her independent laboratory in 1997, she recognized the need for a mouse model of diabetes mellitus–accelerated atherosclerosis that could separate the effects of diabetes mellitus per se from the effects of diabetes mellitus–induced hyperlipidemia. The laboratory created a transgenic mouse that develops type 1 diabetes mellitus in a process similar to that of type 1 in humans, with viral infection inducing T-cell–mediated destruction of beta cells, and also develops atherosclerosis. Using that model, the team showed that, even with no lipid abnormalities or cholesterol in the diet, diabetes mellitus accelerates the initiation of atherosclerotic lesions by stimulating macrophage accumulation within the vascular wall. In contrast, when the mice are fed a cholesterol-rich diet and then given diabetes mellitus, they develop severe hypertriglyceridemia and advanced atherosclerotic plaques.1 Later, when the team induced type 1 diabetes mellitus in mice after they …