In an article entitled, “Betatrophin: A Hormone that Controls Pancreatic β Cell Proliferation,” published in May 9, 2013, issue of Cell (153:747-758), the lead author Peng Yi with two other associates from the Department of Stem Cell and Regenerative Biology, Harvard University have discovered a hormone in mice that prompts to boost their production of pancreatic β cells, the ones that make insulin and are missing or not productive enough in patients with diabetes. The hormone (called β trophin) is present in human metabolic system as well and its discoverers hope that the effect in the human pancreas might be similar.

For years, researchers have sought a way to help the body replace missing β cells in people with diabetes so that they could produce enough insulin on their own. The healthy pancreas can at times boost its production of β cells, both in response to injury and to increased demand for insulin—for example, during pregnancy. Peng Yi and his colleagues were trying to better understand the factors that control that process. In the current study, the researchers administered experimental mice a molecule that blocks the insulin receptor on cells, tricking the body of the animal into reacting as if they needed more insulin and producing more β cells. This rodent reaction was involved in turning on and off a number of genes, and the team identified the one that was activated in the liver and fat tissues. It piqued their interest as a possible hormone gene because it codes for a protein that is excreted by cells. When the researchers injected extra copies of the β trophin gene into the liver of the normal mice, the pancreases in the animal responded by making as much as 30 times more β cells than usual. After a week, the injected mice had more than twice the number of β cells compared to animals that did not get the extra copies of the gene. The increased β trophin gene activity did not seem to cause cells to replicate in other parts of the pancreas or in the  liver or fat tissue. However, the mechanism of action for β trophin is still a mystery. It may act directly or indirectly on β cells to control their proliferation. Identification of the β trophin receptor and/or other possible cofactors will help explain how the liver and fat interact with the pancreas to regulate production of β cell mass. Nonetheless, identification of β trophin as a hormone that can exert control on β cell replication and β cell mass opens a new door to possible diabetes therapy.