This means that changes in fat cell mass are caused mainly by changes in fat cell volume and not in absolute numbers of fat cells.
The study, carried out by Bruce Buchholz - along with colleagues from the Karolinska Institute in Sweden; Humboldt University Berlin, Foundation of Research and Technology in Greece; Karolinska University Hospital; and Stockholm University - applied carbon dating to DNA to discover that the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of fat cells is set during childhood and adolescence.
In the new study, Buchholz analyzed the uptake of carbon-14 in genomic DNA within fat cells to establish the dynamics of fat cell turnover. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index.
Neither fat cell death nor its generation rate is altered in early onset obesity, suggesting a tight regulation of the number of fat cells in obese adults.
The study looked at 687 adults, and researchers found that number of fat cells increases in childhood and adolescence, but levels off and remains constant in adulthood. They looked at whether the number of fat cells changes under extreme conditions, such as drastic weight loss by radical reduction in caloric intake, such as through bariatric surgery. The treatment resulted in a significant decrease in BMI and fat cell volume; however, it did not reduce the number of fat cells two years after the surgery. Similarly, significant weight gain (15-25%) over several months in non-obese adult men resulted in significant increase in body fat volume but no change in number. Subsequent weight loss back to baseline resulted in a decrease in fat cell volume but no change in the number of fat cells.
These results could help researchers develop new pharmaceuticals to battle obesity as well as the accompanying diseases such as high blood pressure and diabetes.
