University College London researchers said the finding adds to a growing body of work showing the importance of insulin signaling pathways as an aging mechanism in mammals, and potentially humans.

The team studied mice engineered to lack either insulin receptor substrate IRS-1 or IRS-2. Those proteins are activated by insulin, a hormone that regulates glucose and fat metabolism, informing the body’s cells when the animal is well fed.

The study showed mice lacking IRS-1 had an average lifespan increase of 20 percent compared with normal mice. In female mice lacking IRS-1 the increase averaged 30 percent. As well as living longer, the mice without IRS-1 also experienced better health than the normal mice as they aged.

In comparison, mice lacking IRS-2 were shorter-lived than the normal mice and displayed signs of obesity and type 2 diabetes.

The research, led by Professor Dominic Withers, is reported in The FASEB Journal.