Silencing a gene involved in the way cells use insulin helps keep the hearts of elderly mice young, according to a new study. The gene, P13K, plays a key role in the proliferation of cells and in the way they age, and the gene has previously been shown to maintain heart health in fruit flies.
In the current study, Tetsuo Shioi and his colleagues at Kyoto University Graduate School of Medicine looked at the hearts of elderly mice who were genetically engineered to have P13K suppressed; the team compared their findings to the hearts of normal elderly mice. They found that the hearts of the mice lacking P13K activity had better overall cardiac function, less fibrosis (thickening of heart tissue), and fewer biological markers of the ageing process than the hearts of the normal mice. The heart tissue of the P13K−suppressed mice also showed a pattern of gene activity that was similar to the hearts of younger mice, compared to the control group.
As to the question of whether the findings may apply to humans, the answer is a likely 'yes.'
Shioi says that “[t]his study showed that aging of the heart can be prevented by modifying the function of insulin and paves the way to preventing age−associated susceptibility to heart failure.”
He also points out, however, that genetically engineering the human heart over the course of a lifetime is just not feasible. As a more practical alternative, he suggests that “drugs that lower insulin are available and can prevent cardiac aging, increase exercise tolerance and reduce heart failure in middle−aged to aged members of the population."
Shioi next plans to study the relationship between insulin and energy intake, since as he says, “caloric restriction is associated with low insulin in blood” and has been associated with lengthening the lifespan in a variety of studies.
The study was published in the online October 12, 2009 edition of Circulation.