GCD student receives Pritzker Scholar Award
Stretched to the limit: Exploring the role of fat cells in metabolic disease
“I really enjoyed the work and felt like I was skilled at it. And when those two things come together, you shouldn’t ignore them.” —Pritzker Scholar Meg Gregor, PhD ‘10
Meg Gregor is growing fat cells in a dish and stressing them out. It’s all part of a typical day’s work in the laboratory of her advisor, Gökhan Hotamisligil, the James Stevens Simmons Professor of Genetics and Metabolism at HSPH. Hotamisligil is pioneering research on obesity’s impact on metabolic diseases, including type 2 diabetes and cardiovascular disease, and the doctoral student is happy to be contributing.
“The research is really intriguing to me because it involves the whole body,” Gregor says. “You focus on what fat cells do, but you also study how fat is affecting the liver or how the brain is affecting your weight.”
Gregor has felt at home in a lab ever since she first stepped into one as a biology undergraduate at Hope College, in Michigan. “I really enjoyed the work and felt like I was skilled at it. And when those two things come together, you shouldn’t ignore them,” she says. A semester abroad in the Dominican Republic, where she shadowed doctors in an urban hospital, opened her eyes to public health.
Asking big questions
After graduation, Gregor worked as a technician at the Van Andel Research Institute in Grand Rapids, Michigan, for four years. There she studied the molecular basis of cancer under distinguished oncologist George Vande Woude, who encouraged her to continue developing as a scientist. At HSPH, where she is working towards a PhD in biological sciences, Gregor, 30, studied under Hotamisligil and became intrigued by metabolic research as it applies to obesity.
Hotamisligil and his colleagues have greatly advanced scientists’ understanding of the biological processes at work in fat cells. Once thought to be mere storehouses for excess energy, fat cells are in fact active players in the system controlling metabolism, the chemical process that converts food into energy. But fat cells can only take so much stress. As Hotamisligil has shown, those of an obese person are stretched to the limit. When faced with additional stresses such as a bombardment of excess nutrients, one of the cell’s chief operating systems, the endoplasmic reticulum (ER), reacts with a stress response that can lead to insulin resistance. This precursor to type 2 diabetes interferes with the body’s ability to process glucose.
New treatment pathways
Gregor’s thesis focuses on how the ER orchestrates fat-cell function. She is also studying the pathways that ignite inflammation in response to the rush of nutrients—a process that scientists now suspect lays the grounds for metabolic disease. Her work has so far generated promising indications that these molecular processes are critical to the health of fat cells, and that it is also possible to enhance their capacity with chemicals that can make the cells more resilient. If these concepts apply to humans (an idea she plans to test), they could open up new possibilities for treating metabolic disease.
“It has been a great joy to work with Meg on this extremely exciting and equally challenging project,” Hotamisligil says. “In general, I like graduate students in the lab to tackle big questions with strong applications to critical health problems. This approach has suited Meg very well; it drives her intellectually and stokes her passion.”
Amy Roeder is the development communications coordinator for the Office for Resource Development at HSPH.? ?