Eliminating old, dysfunctional cells in human fat also alleviates signs of diabetes, researchers from UConn Health report. The discovery could lead to new treatments for Type 2 diabetes and other metabolic diseases.

The cells in your body are constantly renewing themselves, with older cells aging and dying as new ones are being born. But sometimes that process goes awry. Occasionally damaged cells linger. Called senescent cells, they hang around, acting as a bad influence on other cells nearby. Their bad influence changes how the neighboring cells handle sugars or proteins and so causes metabolic problems.

Type 2 diabetes is the most common metabolic disease in the US. About 34 million people, or one out of every 10 inhabitants of the US, suffers from it, according to the Centers for Disease Control and Prevention (CDC). Most people with diabetes have insulin resistance, which is associated with obesity, lack of exercise and poor diet. But it also has a lot to do with senescent cells in people’s body fat, according to new findings by UConn Health School of Medicine’s Ming Xu and colleagues. And clearing away those senescent cells seems to stop diabetic behavior in obese mice, they report in the 22 November issue of Cell Metabolism. Ming Xu, assistant professor in the UConn Center on Aging and the department of Genetics and Genome Sciences at UConn Health, led the research, along with UConn Health researchers Lichao Wang and Binsheng Wang as major contributors. Alleviating the negative effects of fat on metabolism was a dramatic result, the researchers said.

In one of the mysteries of mammalian development, every cell in the early female embryo shuts down one of its two copies of the X chromosome, leaving just one functional. For years, the mechanics behind this X chromosome inactivation have been murky, but scientists from the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have now taken a major step forward in understanding the process.

Their findings, based on research on mouse stem cells, upend previous assumptions about how X inactivation is initiated in female embryos and could lead to new ways to treat some genetic disorders, as well as a better understanding of how genes on other chromosomes are silenced.

“X inactivation is one of the most fundamentally important processes in development, and I think this study is a slam dunk in finally understanding it,” said Kathrin Plath, a professor of biological chemistry and senior author of the paper, published in the journal Cell.

Aging affects everybody, so it’s easy to understand why so much scientific attention is focused on studying it. Scientists in Canada now claim to have found that telomeres play a different role in cellular aging than previously thought.

One of the main points of interest in anti-aging biology are what’s known as telomeres. These are sections of “junk” DNA that form caps on the ends of chromosomes, protecting important genetic information from damage when a cell divides. But a piece of the telomere is eroded away with each cell division, and when it gets too short the cell stops dividing entirely, entering a dormant state known as senescence. The build-up of these senescent cells contributes to a range of symptoms we associate with aging, such as frailty and age-related diseases.

The implication of this model is that telomeres take on a pre-emptive protection role – they signal to cells to stop dividing as soon as one telomere wears out. But there is evidence to suggest that cell division can continue with as many as five dysfunctional telomeres.