Some neurons, which are sensitive for the amount of glucose in blood, appears to play an important roll in the cause of Diabetes mellitus type 2 (adult-onset diabetes). These neurons become active when more glucose appears in the blood, which causes an increase in sugar-uptake. If these neurons are made insensitive, artificially, for glucose, diabetes type 2 will arise.

Now, with this new discovery, scientists have found a method to reverse the onset of too much glucose-uptake. Patients with diabetes type 2 cannot regulate their glucose quality. If the quality after a meal increases, the sugars (or glucose) have be removed, and if the body does not require the glucose for energy supplies, it will be stored in liver and muscles. If this fails, the glucose quality will stay permanent high, which eventually will damage several organs. The uptake of glucose is regulated by the hormone insulin. According to existing conceptions, diabetes type 2 arises if insulin-producing bèta cells in the pancreas fail and liver and muscles become less sensitive for insulin.
Glucose-sensitive neurons are now added as cause.

Physiologists of Boston and Seattle have studied the activity of so-called pro-opiomelanocortin cells (POMC) in the hypothalamus, because these cells are activated by the satiety hormone leptin. These cells are also activated by an increase in glucose quality in the blood, which happens through the glucose sensitive protein.
When deactivated, healthy animals were less capable of taking in glucose from the blood: they got diabetes.
Fattened mice also showed that these neurons were becoming less active, concluding that deviations in POMC can result in diabetes mellitus type 2.

The scientists showed that the enzyme UCP2 will slow down the sensitivity for glucose. When injecting fattened mice with a substance which slows down this enzyme, the diminished sensitivity for glucose of the POMC disappeared.