Researchers have known that reducing food intake without crossing over into the no-go territory of malnutrition can help delay aging and age-associated diseases, but translating those findings into therapeutics has long befuddled drug developers. Now, researchers say deleting a certain gene in mice managed to mimic the benefits of calorie restriction.
After a team of researchers deleted an immune-associated gene called PLa2g7 in laboratory mice, their age-related inflammation declined and metabolic and thymus function improved. The thymus, located above the heart, is crucial to fostering the right microenvironment for T cells, which help fend off infection.
The findings help pinpoint a potential molecular target for lowering inflammation and lengthening a person’s health span without requiring them to restrict their food intake, the Yale School of Medicine researchers reported this month in Science.
A moderate drop in food intake has been shown to delay aging and age-associated diseases in nonhuman primates and other organisms, but translating these findings into targets for new treatments has been a scientific challenge, the team said. Now, with these findings, researchers have more insight into what helps cause the beneficial effects of caloric restriction, the Yale team said.
To identify the gene they decided to test, the Yale researchers looked at immune function in humans who restricted their caloric intake by about 14% over two years, and they evaluated mice that took a more drastic 40% reduction. By analyzing cells and profiling fatty tissue—which is core to energy homeostasis—the researchers found calorie-restricted humans had a reduced expression in the PLa2g7 gene.
Other recent anti-aging research has found that a growth hormone in the colon helps damage DNA, which leads to aging. A team of researchers at Cedars-Sinai Medical Center believes therapies could help offset aging by interfering with the signaling of non-pituitary growth hormones and blocking the growth hormone receptor p53.