One of the characteristic features of the disease type 2 diabetes is the inability of cells of the body to respond to the hormone insulin, something known as insulin resistance.
To determine whether resistance to the effects of insulin on cells in the brain or on cells outside the brain is important for disease, Jens Brüning and colleagues at the University of Cologne, Germany, engineered mice such that when they were given a drug the receptor for insulin was eliminated in either all the cells of the body or only the cells outside the brain.
It was observed that one of the effects of insulin resistance, high levels of glucose circulating in the blood, was more pronounced in the mice in which the receptor for insulin was eliminated in all cells of the body than in the mice in which the receptor for insulin was only eliminated in the cells outside the brain.
The mice lacking the receptor for insulin in all their cells also had less of the white type of fat tissue. Consistent with this, injection of insulin into the brain of normal mice increased the mass of white fat tissue and the size of white fat cells. These data indicate that the cells of the brain mediate some effects in response to insulin that are not mediated by cells outside the brain when they detect the same hormone.
Journal reference: Central insulin action regulates peripheral glucose and fat metabolism in mice. Journal of Clinical Investigation. May 1, 2008.
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