|Mayo Clinic's James Kirkland|
In one of the latest examples of the growing focus on anti-aging research, researchers at the Mayo Clinic have taken what they hope is the first step in reversing age-related stem cell dysfunction and metabolic disease.
Director of the Mayo Clinic Robert and Arlene Kogod Center on Aging and senior author of the study James Kirkland published his group's work in the journal eLife.
"Our work supports the possibility that by using specific drugs that target senescent cells--cells that contribute to frailty and disease associated with age--we could stop human senescent cells from releasing toxic proteins that are contributing to diabetes and breakdowns in stem cells in older individuals," Kirkland said.
They found that human fat cells that deteriorate in old age produce a protein called activin A that leaks into fat tissue and the blood. This protein is thought to impair stem cells found in fat tissue and in turn, the proper functioning of fat tissue.
In an aged mouse model either treated with a Janus kinase (JAK) inhibitor, or genetically engineered to overexpress a drug-activating gene in senescent cells (INK-ATTAC mice), they saw a reduction in activin A and less fat tissue insulin resistance--a consistent feature of aging mice or humans.
In the INK-ATTAC mice, researchers observed an increase in proteins which promoted insulin sensitivity and lowered the risk of the mice developing diabetes.
"The treated animals had improved glucose and insulin tolerance tests, tests that indicate the severity of diabetes
"Our work suggests that targeting senescent cells or their products could be a promising avenue for delaying, preventing, alleviating or treating age-related stem cell and tissue dysfunction and metabolic disease," Kirkland said.
- here's the release
- read the journal abstract