At Yale University, scientists have been studying how fasting can drive the onset of type-2 diabetes. From this research, the scientists have unearthed a novel way of intervening and switching off the process that leads to type-2 diabetes. The research is described in a pair of studies published by Yale medical scientists, with the first focusing on a newly discovered connection between the body’s behavior when it is in a state of fasting, as it is while we sleep, and the development of type-2 diabetes.

The team found that fasting switches on a process whereby two proteins, TET3 and HNF4a, build up in the liver and elevate the production of blood glucose. In a healthy person, this process is switched off when the body exits fasting mode, but in those with type-2 diabetes that off-switch fails, leaving a surplus of glucose to build up in the blood. By coming up with another way to switch it off, the scientists suspected they might be able to stop the disease from developing.

In experiments designed to explore this theory, the team packaged genetic material called small interfering RNAs (siRNAs) inside viruses that target TET3 or HNF4 and injected it into mice. They found that this technique was effective at knocking down the levels of the proteins, along with blood glucose levels, “effectively stopping diabetes in its tracks.”

In the second study, the team explored the role TET3 plays in liver fibrosis, which is a scarring of healthy liver tissue that can lead to life-threatening conditions like cirrhosis. They found that TET3 plays a role at three different points along the fibrosis signaling pathway, meaning that drugs that can target these key proteins in type-2 diabetes could also be leveraged to treat fibrosis, for which there are currently very limited options.

Considering more than 30 million Americans have type-2 diabetes, this new discovery from Yale’s scientists could have a massive impact in the medical world.