Yumi Imai, MD

Contact Information:

Office: 3318 PBDB
Phone: 319-335-4844
Faculty Profile

Brief description of current research:

Dr. Imai’s research aims to understand the mechanism behind pancreatic beta cell failure in type 2 diabetes. Although type 2 diabetes is triggered by insulin resistance due to excessive nutrition, the reduction of functional beta cell mass is ultimately responsible for the inability to maintain glucose homeostasis in type 2 diabetes. Thus, the restoration of healthy beta cell mass is an important goal of diabetes therapy and yet has not been achieved in therapeutics available now. 
Her laboratory currently focuses on how lipid droplet proteins optimize intracellular lipid metabolism to support insulin secretion while preventing beta cells from excessive lipid load. The exposure of beta cells to lipids are known to enhance insulin secretion acutely, while the prolonged exposure leads to beta cell dysfunction and apoptosis. Dr. Imai’s laboratory has revealed that lipid droplet protein perilipin 5 plays an important role in supporting insulin secretion through the regulation of intracellular lipid metabolism. Her laboratory works on the molecular target by which perilipin 5 augments insulin secretion. In addition, her team has been studying mice deficient of perilipins in beta cells as a model of beta cell dysfunction associated with over–nutrition. She is also extending her work of perilipins to other tissues with active lipid metabolism such as the liver considering that the excessive lipid accumulation in the liver (NAFLD) is closely associated with obesity and diabetes. 
An additional area of her research interest includes islet inflammation that is also considered to play a role in beta cell loss in type 2 diabetes. Her research team has utilized human islets and pancreas from non-diabetic and diabetic organ donors to dissect sequence of events during the progression of beta cell failure in diabetes. 
Ultimately, her research team seeks to combine knowledge from key projects to identify a new target to improve beta cell health and function as a treatment for diabetes.


 3 most influential diabetes/obesity/metabolism publications:



  • Imai Y, Varela GM, Jackson MB, Graham MJ, Crooke RM, Ahima RS. Reduction of hepatosteatosis and lipid levels by an adipose differentiation-related protein antisense oligonucleotide. Gastroenterology. 2007;132(5):1947-54.
  • Butcher MJ, Hallinger D, Garcia E, Machida Y, Chakrabarti S, Nadler J, Galkina EV, and Imai Y. Association of proinflammatory cytokines and islet resident leucocytes with islet dysfunction in type 2 diabetes. Diabetologia. 2014;57(3):491-501.
  • Trevino MB, Machida Y, Hallinger DR, Garcia E, Christensen A, Dutta S, Peake DA, Ikeda Y and Imai Y. Perilipin 5 Regulates Islet Lipid Metabolism and Insulin Secretion in a cAMP-Dependent Manner: Implication of Its Role in the Postprandial Insulin Secretion. Diabetes. 2015;64(4):1299-310.





As a physician-scientist, I have been actively involved in both basic research and patient care. I have seen physical, financial, social and emotional tolls of diabetes on patients. Clearly, the current therapeutics are far from sufficient for the treatment of diabetes. Also, I am familiar with heterogeneity in clinical presentations of diabetes, which is likely reflective of complexed disease process. As a member of FOE Diabetes Research Center, I hope to contribute to our goal of advancing diabetes research through my expertise from both research and clinical sides.