SAN DIEGO, Aug 27 (XINHUA/APP):U.S. researchers have found that DNA sustains more damage and gets fixed less often when blood sugar levels are high compared to normal and healthy levels, offering an answer to why people with diabetes have an increased risk of cancer.
The new study was presented at the 2019 national meeting and exposition of the American Chemical Society (ACS), one of the largest scientific conferences of the year, which kicked off on Monday in San Diego, California.
“It’s been known for a long time that people with diabetes have as much as a 2.5-fold increased risk for certain cancers,” said John Termini, who is at City of Hope, a research and treatment center for cancer and diabetes. These include ovarian, breast and kidney cancers, among others.
“As the incidence of diabetes continues to rise, the cancer rate will likely increase, as well,” Termini said.
Scientists have suspected that the elevated cancer risk for diabetics arises from hormonal dysregulation.
“In people with type 2 diabetes, their insulin is not effectively carrying glucose into cells,” Termini explained. “So the pancreas makes more and more insulin, and they get what’s called hyperinsulinemia.”
In addition to controlling blood glucose levels, the hormone insulin can stimulate cell growth, possibly leading to cancer. Also, most people with type 2 diabetes are overweight, and their excess fat tissue produces higher levels of adipokines than those at a healthy weight. These hormones promote chronic inflammation, which is linked to cancer.
Termini believed the elevated blood glucose levels seen in diabetes could harm DNA, making the genome unstable, which could lead to cancer.
Termini and his colleagues looked for a specific type of damage in the form of chemically modified DNA bases, known as adducts, in tissue culture and rodent models of diabetes. Indeed, they found a DNA adduct, called N2-(1-carboxyethyl)-2′-deoxyguanosine, or CEdG, that occurred more frequently in the diabetic models than in normal cells or mice.
They identified two proteins that appear to be involved: the transcription factor HIF1a and the signaling protein mTORC1, which both show less activity in diabetes. HIF1a activates several genes involved in the repair process.
According to Termini, several drugs that stimulate HIF1a or mTORC1 already exist. The researchers plan to see if these drugs decrease cancer risk in diabetic animal models, and if so, they will test them in humans.
More than 9,500 presentations will be delivered during the ACS conference which will last until Thursday, related to the theme of “Chemistry and Water.”