Washington, June 6 (ANI): A researcher has said that new findings about the biological links between obesity, insulin resistance and type 2 diabetes may could also help shed light on the connection between obesity and cancer.
In the study, UT Dallas' Dr. Jung-whan (Jay) Kim and colleagues at the University of California, San Diego found that a protein called HIF-1 alpha plays a key role in the development of insulin resistance and type 2 diabetes in obese mice
The researchers genetically engineered mice to lack the HIF-1 alpha protein within the animals' fat cells, or adipocytes. The animals still made HIF-1 alpha in other types of cells and tissues in their bodies.
Although the mice became obese when fed a high-fat diet, they did not develop insulin resistance and diabetes to near the extent that genetically normal, obese mice did.
Kim, a co-lead author of the study who conducted the research while a postdoctoral researcher at UC San Diego and the Salk Institute for Biological Studies, said that there is clearly a greater chance among the obese human population to develop insulin resistance and diabetes.
Kim said the findings about HIF-1, which stands for hypoxia inducible factor-1, are significant not only for their possible application to fighting insulin resistance and diabetes, but also cancer. Here's why:
To study the effect HIF-1 alpha might have on the development of insulin resistance and diabetes, Kim and his colleagues used genetic engineering techniques to completely remove, or "knock out" HIF-1 alpha from adipose tissue in obese mice.
He said tumor cells grow really fast, but the blood vessels that feed them oxygen cannot grow fast enough, so tumor cells become hypoxic, adding that the tumor cells have to develop some sort of mechanism to survive under hypoxic stress, and that's HIF-1 alpha.
Kim said that if one can inhibit HIF-1 alpha in a tumor cell, one can kill the cell, and that's why pharmaceutical companies are interested in HIF-1 inhibitors.
The study has been published online in the journal Cell. (ANI)