Investigating the causes of beta cell dysfunction in type 1 diabetes

Type 1 diabetes (T1D) occurs when the immune system misguidedly attacks and destroys beta cells in the pancreas. Beta cells normally produce insulin, a chemical messenger that helps move sugar from food sources into cells throughout the body, which use it for fuel to stay alive. Without adequate insulin, blood glucose levels rise too high and can cause serious damage to all organs.

Dr. Heather Denroche at the University of British Columbia is currently examining a hormone called islet amyloid polypeptide (IAPP), produced by pancreatic beta cells and released in response to elevated glucose, in order to better understand the role it plays in the loss of beta cells leading to T1D, as well as in transplanted stem cell-derived beta cells.

Recent findings reveal that deposits of IAPP attract immune cells and cause inflammation. Dr. Denroche is investigating how this process occurs, and whether or not it influences the development of T1D and the outcome of beta cell transplants.

“Both the immune system and the pancreatic beta cells actively contribute to the underlying causes of T1D,” explains Dr. Denroche. “With support from JDRF, this research will advance our understanding of how IAPP, a beta cell-derived factor, participates in the progression of the disease, potentially leading to novel strategies to prevent or better treat diabetes in the future.”

“Heather is a brilliant young scientist who has brought new ideas and energy to this exciting project,” says Dr. Bruce Verchere, director of the Centre for Molecular Medicine and Therapeutics at the University of British Columbia. “We are both very appreciative of her JDRF advanced post-doctoral fellowship support, which not only allows her to pursue this work, but is also a steppingstone towards starting her own diabetes research laboratory in a few years.”

Better characterization of IAPP as a potential therapeutic target to prevent T1D progression and maximize the success of beta cell transplantation could advance knowledge needed for improved treatment of T1D and possibly even inform a cure.

 

Lets turn type one into type none