According to a report in the September 30th issue of the Cell Press journal, Cell, a pathway that initially drew attention for its role in embryonic stem cells and cancer also influences the odds that mice develop or resist diabetes.
Mice with high levels of the cancer-promoting proteins Lin28a or Lin28b become more sensitive to insulin and less prone to diabetes when on a high-fat diet, the new study shows.
“This highlights the overlap in the biology of these disorders,” said George Daley of Harvard Medical School. “It may be the same kinds of metabolic shifts that allow cancer cells to grow are also related to [whole-body] glucose metabolism.”
In fact, there were clues about such a connection, but “no obvious mechanism,” he says. For instance, studies have shown that cancer cells within a tumor are able to grow more rapidly by shifting the way they use glucose. Genome-wide association studies for type 2 diabetes have also pinpointed several susceptibility genes with known links to cancer or the cell cycle.
Daley’s team, including first authors Hau Zhu and Ng Shyh-Chang, had noticed earlier that an immature form of the microRNA (tiny bits of RNA that silence genes by targeting messenger RNA) known as let-7 is abundant in stem cells. “It allows stem cells to be stem cells,” Zhu says.
Article source: http://www.medindia.net/news/Shared-Biological-Basis-of-Diabetes-and-Cancer-91364-1.htm