Mice lacking a gene had fewer signs of aging in fat tissue
At 10 months, male mice lacking the gene had greater activity in mitochondria, the cells’ energy-producing structures, than mice retaining it.
Limit: The experiments used gene deletion, not a drug targeting HDAC9
Edited by Boris Djordjevic · AgingResearch.News
Researchers compared male mice lacking the gene for histone deacetylase 9, a protein that regulates fat-cell development, with littermates retaining it. This animal experiment used mice fed standard chow. At 12 months, mice lacking the gene had less fat and fewer signs of senescence, a state in which cells stop dividing, in fat tissue.
At 10 months, mice lacking the gene had more mitochondrial DNA and higher oxygen use at rest in fat beneath the skin. Mitochondria are the cells’ energy-producing structures. Gene deletion also raised levels of an enzyme called thiosulfate sulfurtransferase. In mouse fat-cell precursors grown in the lab, reducing this enzyme increased senescence markers. The authors concluded that gene deletion reduced age-related fat-tissue senescence and mitochondrial dysfunction, at least partly by increasing this enzyme.
Why it matters
Age-related senescence and mitochondrial dysfunction in fat tissue can disrupt the body’s metabolic balance. The authors suggest that targeting this gene may help maintain healthy fat tissue during aging.
Caveats
The experiments tested genetic deletion, not a drug targeting the protein. Most experiments used male mice, and the results do not establish benefits in people.
