Researchers were able to extend lifespan in mice by up to a fifth and reduce the number of age-related diseases the animals suffer by blocking a key molecular pathway.
The research mimics the health benefits of reducing calorie intake, and suggests that drug treatments for ageing and age-related diseases are feasible.
For a long time, "calorie restriction" appeared to increase the life span of the animals, and a recent study showed that this might be the case for primates, although they have not uncovered the reason behind the phenomenon.
Evidence also suggests that calorie restriction can have health benefits for humans, too, though it is unclear whether it can increase longevity.
In the new study, researchers from the Institute of Healthy Ageing at UCL (University College of London) have discovered changes in the ageing process in a strain of knockout mice, which were unable to produce a particular protein known as S6 Kinase 1 (S6K1).
S6K1 is involved in the body's response to changes in levels of the food that we eat.
Professor Dominic Withers and colleagues demonstrated that deleting the S6K1 protein in mice has a wide range of health benefits, which appear to mimic the action of calorie restriction.
However, the researchers observed that whilst the effect was dramatic in female mice, their male counterparts showed little difference in lifespan but showed some of the health benefits.
But, the reasons for these differences between the two sexes are unclear.
"Blocking the action of the S6K1 protein helps prevent a number of age-related conditions in female mice. The mice lived longer and were leaner, more active and generally healthier than the control group. We added 'life to their years' as well as 'years to their lives,"' said Withers.
On average, the female knockout mice lived for 950 days, over 160 days longer than the control group - in other words, their lifespan increased by twenty per cent.
The findings suggest that calorie restriction acts via the S6K1 pathway.
Further studies showed that the beneficial effects of blocking S6K1 were mediated via increased activity of a second molecule, AMPK which has been called a master 'fuel gauge' as it regulates energy levels within cells.
It is particularly activated when cellular energy levels fall such as can occur when calorie intake is reduced.
Drugs that activate AMPK are already in use in human patients to treat type 2 diabetes - metformin, a widely-used drug for the disease, is thought to work by activating AMPK.
Recent Russian studies appear to show that the drug can extend the life-span of mice.
A recent study showed that the drug rapamycin extended the lifespan of mice, while rapamycin blocks the activity of S6K1 and may therefore extend lifespan through its effects on S6K1.
Thus, the findings offer evidence that this is a drug-sensitive pathway controlling mammalian ageing and suggest new approaches for the treatment of age-related diseases.
The results of the study have been published in the journal Science.