doi:10.1038/nindia.2013.36 Published online 20 March 2013
Researchers have found that aging fat cells could signal diabetes. In a new research, they show that aging fat cells provide a molecular link to a person's insulin resistance, a precursor for many metabolic diseases including diabetes1.
The researchers have shown in animal models that it is possible to selectively target aging cells, eliminate them and delay or prevent age-related pathologies. This calls for further research on 'clearing away old cells' either pharmacologically or by lifestyle modifications to achieve healthy aging.
In response to a variety of stress signals, including nutrient deprivation, oxidative stress, dysfunctional telomeres and DNA damage, normally dividing cells can permanently withdraw from the typical cell cycle. These cells are then said to be in a state of 'cellular senescence', where their capacity to replicate is destroyed. Growing evidence suggests that these senescent cells contribute to aging in a variety of organisms, including mice and humans.
Senescent cells lurk in our tissues. They escape elimination due to impaired programmed cell death or altered immune surveillance. Senescent cells have been reported to behave badly, secrete chemicals that degrade surrounding tissue and harm neighboring cells. Their increasing omnipresence contributes to accelerated aging and age-related pathologies.
"In our study, fat cells subjected to oxidative stress became senescent associated secretory phenotype (SASP), started signalling proinflammation, exhibited shortened telomeres and became insulin-resistant. This is a hallmark characteristic of diabetes" says lead author Muthuswamy Balasubramanyam.
"We need to find a robust way of identifying senescent cells and selectively removing them. This should pave way for either prevention or delaying of age-related pathologies including diabetes" he adds.
The authors of this work are from: Madras Diabetes Research Foundation and Dr. Mohan's Diabetes Specialities Centre, Chennai, India.