Earlier studies showed that Pax4 was important for making insulin-producing cells in the pancreas, Mansouri explained. Mice without the gene die at birth with pancreases that look normal except that they lack beta cells.

The researchers also found previously that another factor, which works against Pax4 action, could turn beta cells into alpha cells. (Alpha cells produce a hormone called glucagon when blood sugar levels fall too low, causing the liver to release glucose from storage.)

The discovery suggested to them that the opposite conversion might also be achieved. And indeed, they now show that it can. Mice with Pax4 switched on in the pancreatic cells end up with an eight-fold increase in the number of beta cells, Collombat said.

Those beta cells seem to be fully functional, they report. In mice treated with a drug that selectively kills beta cells, the conversion of alpha into beta cells can counter the effects of their diabetes, at least when the mice are treated at a young age.

Further studies are needed to show that the alpha to beta cell conversion can be kept under control, Mansouri said.

"Too many beta cells isn't good either," he said. "We'll need a strategy to trigger Pax4 and, at a certain point, also stop it."

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