One of the main mysteries about diabetes is why specialized cells in the pancreas discontinue secreting insulin. Apparently, the body requires insulin in order to store glucose from food.
A team from the Children’s Hospital of Eastern Ontario (CHEO) Research Institute seems to have identified a protein which inhibits insulin production in mice. This latest study may possibly offer a novel way of understanding and perhaps one day treating both Type 1 and Type 2 diabetes.
During the study, experts were noted to have utilized sophisticated genetic engineering in order to remove or ‘knock out’ the Lkb1 gene from beta cells of laboratory mice.
Lead author of the study, Dr. Robert Screaton, who holds the Canada Research Chair in Apoptotic Signaling at the University of Ottawa, stated that, “We were surprised by the impressive accumulation of Lkb1 in beta cells of diabetic mice, which suggested that Lkb1 might contribute to their impaired function. After removal of the Lkb1 gene, the beta cells grow larger, proliferate more, and secrete more insulin. It’s a one-stop shop for the much needed insulin. The knockout mice on a high fat diet have lower blood glucose. If this observation is confirmed in humans, it may give us another clue into the development of Type 2 diabetes, and perhaps new treatment options.”
Dr. Alex MacKenzie, CEO of the CHEO Research Institute and a physician who treats children with diabetes at CHEO stated that, “Type 1 and 2 diabetes, already common diseases, is showing disturbingly steady growth in incidence. The two conditions are among Canada’s, and indeed the globe’s, greatest health challenges. The findings of Dr. Screaton’s team introduce a novel and unanticipated potential therapeutic avenue for this costly and serious condition. It is some of the most important work to come out of our institute.”
They discovered that there seems to be an increase in both the size and number of beta cells. Moreover, there appeared to be greater amounts of insulin stored and released by the cells.
Significantly, the improved beta cell function was believed to have lasted for at least five months, even in mice which were fed a high-fat diet. Supposedly, this high-fat diet was designed in order to mimic the high caloric intake associated with Metabolic Syndrome and Type 2 diabetes in humans.
The findings of the study have been published in the journal, Cell Metabolism.