LIVERMORE, Calif. Beta cells, which make insulin in the human body, do not replicate after the age of 30, indicating that clinicians may be closer to better treating diabetes.
Type 1 diabetes is caused by a loss of beta cells by auto-immunity while type 2 is due to a relative insufficiency of beta cells. Whether beta cells replicate after birth has remained an open issue, and is critically important for designing therapies for diabetes.
By using radioactive carbon-14 produced by above-ground nuclear testing in the 1950s and '60s, researchers have determined that the number of beta cells remains static after age 30.
Lawrence Livermore National Laboratory scientist Bruce Buchholz, with collaborators from the National Institutes of Health, used two methods to examine adult human beta cell turnover and longevity.
Using LLNL's Center for Accelerator Mass Spectrometry, Buchholz measured the amount of carbon 14 in DNA in beta cells and discovered that after age 30, the body does not create any new beta cells, thus decreasing the capacity to produce insulin as a person ages.
Carbon 14 atmospheric concentration levels remained relatively stable until the Cold War, when above-ground nuclear bomb tests caused a sharp increase, or peak, which decreased slowly after the end of above-ground testing in 1963. This spike in carbon 14 in the atmosphere serves as a chronometer of the past 57 years.
Because DNA is stable after a cell has gone through its last cell division, the concentration of carbon 14 in DNA serves as a date mark for when a cell was born and can be used to date cells in humans
"We found that beta cells turnover up to about age 30 and there they remain throughout life," Buchholz said. "The findings have implications for both type 1 and type 2 diabetes."
Type 1 diabetes is an auto-immune disease in which the body attacks beta cells. Both genetic predisposition and environmental triggers th
|Contact: Anne Stark|
DOE/Lawrence Livermore National Laboratory