Endocrine News talks to Michael W. Schwartz, MD, the 2022 Laureate recipient of the Roy O. Greep Award for Outstanding Research about his life and career in academic research that all started with a fascination with how the brain controls behavior.
With his significant contributions in uncovering how our brain regulates energy balance and glucose metabolism, Michael W. Schwartz, MD, is credited for helping to develop novel solutions in the battle against obesity and diabetes. As recipient of the Robert H. Williams Endowed Chair in Medicine, Schwartz was the founding director of the University of Washington Medicine Diabetes and Obesity Center of Excellence and guided the transition of this program into the UW Medicine Diabetes Institute, which he currently co-directs.
The Endocrine Society has honored Dr. Schwartz as this year’s recipient of the Roy O. Greep Laureate Award for Outstanding Research. In his lab of 15 to 20 team members, Schwartz is currently working to unravel the mystery of how fibroblast growth factor (FGF) family members, including FGF19, FGF21 and FGF1, improve glucose metabolism through actions in the brain.
Endocrine News spoke with him to learn more about his life’s path to his research work and what he hopes might be the next scientific breakthrough that could change the lives of patients living with type 2 diabetes.
Endocrine News: The Laureate award is named in honor of Roy O. Greep, PhD, the Endocrine Society’s 45th president and a renowned researcher. What did news of the recognition mean to you?
Schwartz: I am humbled and honored to receive this recognition. Dr. Greep was among the great pioneering leaders in endocrine research, and he also served as president of the Endocrine Society during its formative years. At that time, the Society had distinguished itself from other medical organizations — and still does — by its unwavering commitment to science and to an evidence-based understanding of how the body works, and how that information can be translated to effective, mechanism-based treatment of human disease. That same commitment has guided me throughout my career.
EN: Was there a defining moment early in your career that sparked the trajectory into diabetes and obesity research?
Schwartz: I first became interested in how the brain controls behavior during my undergraduate years at the University of Colorado, a fascination that persisted throughout my years in medical school and medical residency. The fundamental question that motivated me was, “how can a collection of neurons or neurocircuits provide an individual with perceptions, motivations, and awareness?”
As I began my fellowship training in endocrinology, I realized that this type of question can be pursued in very mechanistic terms by trying to understand how the brain links changes in nutritional state to adaptive changes in the drive to eat. That question was at the heart of my decision to pursue a career in academic research at the beginning of my fellowship.
In terms of my hopes for the future, growing evidence from our group and others suggests that the brain works in partnership with pancreatic islets and other peripheral tissues to orchestrate adaptive changes in how glucose is used in the body, and in so doing, helps to maintain the blood glucose level within a normal physiological range.
EN: What research goals are you targeting for the next five to 10 years? Is there one specific therapeutic breakthrough you hope type 2 diabetes patients can experience in the next decade by your peer researchers across the globe?
Schwartz: In terms of my hopes for the future, growing evidence from our group and others suggests that the brain works in partnership with pancreatic islets and other peripheral tissues to orchestrate adaptive changes in how glucose is used in the body, and in so doing, helps to maintain the blood glucose level within a normal physiological range. I suspect we will eventually learn that a critical component of this regulatory system involves the brain’s capacity to sense the circulating glucose level, and to then transduce this afferent information into adaptive responses that promote metabolic homeostasis.
I also anticipate that we will discover that defects in this sensing process are fairly common, and that when they occur, they can raise the defended blood glucose level into the diabetic range, thereby playing a key role in the pathogenesis of type 2 diabetes. Perhaps one day, therapeutic strategies aimed at reversing such defects can be used to restore the defended blood glucose level to normal in these patients(rather than simply lowering the glucose level, as might be achieved by insulin injection, for example). Indeed, we have already shown that this is possible in rodent models of type 2 diabetes.
—Fauntleroy Shaw is a freelance writer based in Carmel, IN. She is a regular contributor to Endocrine News.
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