The study appears online and is scheduled for later print publication in the Journal of the Federation of American Societies for Experimental Biology.
This research applies only to non-insulin-dependent diabetes mellitus and not Type 1 diabetes, which occurs when the pancreas does not produce enough insulin. Not all people with Type 2 diabetes have a shortage of insulin, but their bodies do not respond correctly to the hormone.
Insulin is responsible for transferring sugar, or glucose, from the blood into the cells to be used for energy. When people become insulin resistant, the main characteristic of Type 2 diabetes, that process does not function properly, which tends to drive up blood sugar levels and starve cells of energy.
Many current diabetes drugs stimulate the body to release more insulin or otherwise act in a way that affects sensitivity to insulin. A drug targeting MIF could offer different benefits by lowering blood sugar and inflammation without the need to generate more insulin, Satoskar noted.
Satoskar and colleagues induced Type 2 diabetes in two groups of mice: normal mice and those lacking MIF. They induced the disease by injecting them one time with a naturally occurring toxin, streptozotocin, which acts on cells in the pancreas.
Researchers collected blood samples from the mice multiple times over 10 weeks, conducted oral glucose tolerance tests, and monitored their weight and urine output.
All animals with induced disease showed a spike in blood sugar levels shortly after the injection of the toxin, but the blood sugar levels continued to rise in the normal diabetic mice. These mice also took in more food, lost weight and produced excessive amounts of urine all symptoms associated with insulin resistance.
Mice lacking the MIF protein, on the oth
|Contact: Abhay Satoskar|
Ohio State University