Experiments which mimicked a low-calorie diet by tinkering with genes in mice extended their lives and prevented disease, and a drug that has the same effect could give people longer, healthier lives, scientists said on Thursday.

British researchers found that deleting a gene linked to nutrients and growth helped mice to live 20 percent longer on average, and partly explained why eating less appears to improve health and increase longevity.

The findings also offered a possible genetic drug target for protecting against aging-related diseases, they said.

What we have shown is that this gene is one that regulates life span and also determines how healthy animals are in middle and late age, said Dominic Withers of the Center for Diabetes and Endocrinology at University College London.

Withers and his colleagues used so-called knockout mice -- mice bred with a certain gene removed or knocked out -- in this case the ribosomal S6 protein kinase 1 (S6K1) gene.

Deleting S6K1 meant the mice's bodies behaved in a similar way to mammals whose calorie intake is restricted, they said.

These mice were resistant to type 2 diabetes ... and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis -- so they had stronger bones, Withers said.

Balance, strength and coordination all improved in the knockout mice, and they were more inquisitive, suggesting their brains were healthier.

Our results demonstrate that S6K1 influences healthy mammalian life span, the researchers wrote in their study published in the journal Science.

Most calorie restriction studies have found that a lifetime of deprivation is needed to achieve the longer-life benefits, and many researchers are working on ways to replicate the findings with drugs.

Withers said he knew of various pharmaceutical companies looking at developing drugs that could manipulate the S6K1 pathway, and his study showed they may also prove useful in age-related diseases, assuming they are safe in the long term.

But he also noted that his study had shown that another well-known target, known as AMP-activated protein kinase or AMPK, was on the same pathway as S6K1, meaning existing drugs could be explored to see if they might have the same effect.

Metformin -- a common diabetes drug that works by stimulating AMPK, a master circuit for energy metabolism in the body -- could be examined in this context, he said.

Since people live far longer than mice, it is almost impossible to study fully the effects of restricting calories in humans, but this study in mice and another recently in monkeys offer good clues for humans, Withers said.

The big implication is that intervening in aging protects against a broad spectrum of aging-related diseases, and there is now a druggable pathway providing a means to do this which could be used, in principle, in people, he said. 

Researchers reported in August that the antibiotic rapamycin, sold by Wyeth under brand Rapamune to suppress the immune system in transplant patients, showed promise at slowing age-related disease in older mice, but it is not clear how it works.