Hormone that makes diabetes-fighting cells in mice holds promise for humans

Beta cell expert Philip diIorio eager to apply findings to future studies

By Sandra Gray

UMass Medical School Communications

May 01, 2013
diiorio-philip
Philip diIorio, PhD

Developmental biologist Philip dilorio, PhD, believes the recent discovery of a hormone that accelerates the growth of insulin-producing beta cells in mice may offer new hope for treating type 2 diabetes in humans.

“Any mechanisms we can explore—like the one outlined in this paper—is one step forward in understanding human beta cells,” said Dr. diIorio, research assistant professor of molecular medicine, who studies the genetics and physiology of these cells in the Diabetes Center of Excellence at UMass Medical School. “It gives us a completely new protein and a new pathway that could be looked at in humans as well.” diIorio was not part of the study, which was conducted at Harvard.

The identification of a gene in the liver of insulin-resistant mice that produces a hormone which, in turn, stimulates rapid reproduction and growth of insulin-producing beta cells, was published in the journal Cell last week. The researchers named the hormone “betatrophin” and, while cautioning that more research needs to be done, hope that its discovery will lead to the development of a treatment that can regulate blood sugar in humans better than insulin and other medications.

”Basic research is linked to clinical therapies through these kinds of investigations,” said diIorio about why the study is generating so much interest. Beta cells, which develop in the pancreas, secrete precisely calibrated amounts of insulin in response to varying glucose levels in the blood. In type 2 diabetics, beta cells are present but do not function properly. “There is recognition that at some point we are going to need to make beta cells, whether within a patient, which we call regeneration, or in a dish, for transplantation,” he said.

diIorio studies how beta cells develop in humans. “I was impressed because it’s not an easy thing to track down a signal that’s coming from another organ,” noted diIorio, who focuses on the pancreas, in which beta cells actually form. “Here is a protein in the liver affecting the pancreas, so it highlights how little we still know about how organs interact.” Acknowledging that some related research has been disappointing, diIorio nonetheless feels the betatrophin study underscores the importance of patience and optimism in scientific research.

diIorio and colleagues in the Diabetes Center of Excellence look forward to applying the betatrophin findings to their ongoing studies of the development and function of human pancreatic beta cells, and how they interact with the immune system. “We’d love to start working with the betatrophin in vitro to see its effect on human beta cells, and we’d love to look at human beta cell development and see if betatrophin is expressed at all in the developing pancreas,” he said. “Studies like these motivate us to re-evaluate what we’re looking at and get going in new directions.”