Two research studies being released this
week by scientists at Joslin Diabetes Center and their colleagues suggest two locations in the insulin signaling system that may result in type 2 diabetes
and several conditions frequently associated with this form of diabetes,
namely the inability to control appetite, obesity and even infertility.
One paper, being published today in the journal Science, suggests that
when the insulin receptor in the brain is shut off through genetic
alterations, the mice also develop type 2 diabetes, their appetites are
increased, they gain weight, and their reproductive capabilities decline.
The other paper, published yesterday in the journal Nature, suggests
that when IRS-2 -- a protein inside cells and involved in the insulin
signaling process -- is shut off through genetic alterations, the mice develop
type 2 diabetes, their appetites increase, they gain weight and their
reproductive capabilities decline.
Together these papers demonstrate a previously unappreciated role of the
brain in control of metabolism and of insulin in control of reproduction.
Although many scientists have long thought that insulin was largely
inactive in the brain, more recent studies have begun to unravel this
hypothesis. In both papers, this decline in reproductive abilities and
increased weight gain and appetite occur in a much more pronounced way in the
female mice than in the male mice. The insulin receptor plays a role in
insulin signaling in all tissues, where as the effects of IRS-2 are most
important in the liver, beta cells of the pancreas and brain.