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.
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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.