New findings from studies in mice suggest that defects in the brain's ability to respond to glucose play a role in the development of non-insulin dependent (type 2) diabetes, and that a high-fat diet may contribute to impairing brain cells' ability to regulate glucose throughout the body.
The new study, led by researchers at UT Southwestern Medical Center, Harvard Medical School and Oregon Health and Science University, is the first to demonstrate the mechanisms by which certain glucose-activated neurons respond to glucose, as well as the overall physiological role of glucose-sensing in these neurons, said Dr. Roberto Coppari, assistant professor of internal medicine at UT Southwestern and co-lead author of the study appearing online in the journal Nature.
In the 1960s, scientists discovered that certain neurons in the brain are activated by glucose. The physiological relevance of such neuronal glucose-sensing, and its underlying cellular mechanisms, have been elusive, however.