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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.

The Food and Drug Administration approved the first treatment for the most common cause of dwarfism Friday, a drug that has proved to increase children’s height but has been polarizing among adults with short stature.

The treatment, developed by BioMarin Pharmaceutical, is a once-daily injection for children with achondroplasia, a rare genetic disorder that results in dwarfism and can lead to serious medical complications. In a pivotal clinical trial, patients who got the drug, called Voxzogo, grew 1.6 centimeters more over the course of a year than those who received placebo. That means patients who take Voxzogo throughout childhood are likely to reach heights similar to their peers who don’t have achondroplasia, according to BioMarin.

“It’s the difference between being able to drive a car or not, reaching stuff in closets, being able to take care of your hygiene,” said Jean-Jacques Bienaimé, BioMarin’s CEO. “It would make a huge difference for those patients. There’s no question about it.”

Some Drosophila species have cryptic sex-ratio drive systems. Here, the authors show rapid expansion of a driver gene family, Distorter on the X, in three closely related Drosophila species on the X chromosome and suppressors on the autosomes.

The development of a genetic code expansion-based system enables fast protein expression in response to a noncanonical amino acid. The system was implanted into diabetic mice to rescue hyperglycemia with oral delivery of the amino acid.

In an unprecedented atlas, researchers begin to map how genes are turned on or off in different cells, a step toward better understanding the connections between genetics and disease.

Researchers at University of California San Diego have produced a single-cell chromatin atlas for the human genome. Chromatin is a complex of DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

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.

One-minute-long excerpt of the intervention of Professor David Sinclair during an event organized by the SALT Fund, that took place in October.

In this excerpt, Professor Sinclair talks about the work done in his Lab at Harvard University on partial cellular reprogramming and rejuvenation.

Continue reading “David Sinclair on partial cellular reprograming and rejuvenation (with S/T in Spanish)” »

A model of facilitated diffusion and the theory of Anderson localization help explain how the Cas9 protein explores DNA in search of its targets.

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.