The levels of blood glucose are regulated by the hormone insulin. In type II diabetes, it is the tissues of the body, such as skeletal muscle, that no longer respond correctly to the insulin signal. The research team demonstrated that the absence of Id2 results in the opposite effect, in which the Id2 knockout mouse has an enhanced sensitivity to the insulin signal. This subsequently increases uptake of glucose in the body's tissues and depletes the blood of glucose, resulting in hypoglycemia.
The study also revealed differences in the quantities of fat molecules stored within the skeletal muscle of the Id2 knockout mice. The diacylglycerol molecules (a glycerol molecule bound to two fatty acid molecules) that can accumulate in skeletal muscle are considered important modulators of insulin signaling.
"Since we observed differences in both overall quantities between the sexes, and in the relative proportions of different diacylglycerol sub-types in the male Id2 knockout mice highlights a possible mechanism through which Id2 could be changing the sensitivity of muscle to the insulin hormone signal," Duffield added.
"The circadian clock and energy metabolism systems are tightly linked, one regulating the other," Duffield said. "These and our previously published studies suggest as important role for the Id2 gene in shaping aspects of both of these systems. What our new study reveals is an important contribution for this gene in how the body controls blood glucose levels and metabolizes glucose, as well as how timing of feeding is regulated by the circadian clock. As feeding and fasting and the biological drive to eat are critical aspects of the daily metabolic cycle, these aspects are very much interconnected. What these data and some of our earlier work really mean for the human is that Id2 could serve as a p
|Contact: Giles Duffield|
University of Notre Dame