A new experiment showed that removing certain genes in mice could imitate the effects and benefits of low-calorie diets such as extended lives and prevention of diseases. Scientists said that a drug, which may have similar effect on genes, could help people live longer and healthier lives.
British researchers discovered that removal of a gene associated with nutrients and growth allowed the mice to increase their lifespan by 20 percent, justifying why eating less is better for your health and can increase longevity. A drug that could target this specific gene can also combat aging-related diseases.
“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.
The mice were bred by removing the ribosomal S6 protein kinase 1 (S6K1) gene that allowed their bodies to conduct in a “similar way to mammals whose calorie intake is restricted,” said the researchers.
“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.
Not only were the mice treated by an experimental condition that enable them to live longer, but they also had improved balance, strength, coordination, suggesting a healthier brain. “Our results demonstrate that S6K1 influences healthy mammalian life span,” the researchers wrote in their study.
In the past, studies about calorie restrictions have discovered that eating less does have long-term benefits and many researchers are hoping to replicate their findings in people through drugs. Withers knew of many pharmaceutical companies attempting to manipulate the S6K1 pathway, hoping that it would prevent age-related diseases, if the treatment or drug were safe.
A similar gene, the AMP-activated protein kinase, AMPK was also on the same pathway as S6K1, suggesting that current drugs which target the AMPK may also produce similar results of increased longevity and improved health. Metformin, a common diabetes drug which stimulates the AMPK, could be used to test this hypothesis.
However, since there is a difference between lifespan of mice and human beings, researchers are uncertain about the extent to which the drugs would affect human health and lifespan. But the researchers remain hopeful as Withers said that the study has been conducted in mice and monkeys and has the potential to offer clues into the human functions.
“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.