But although it may be bad for kids, it may be good for type 2 diabetics; a recent report in Nature Medicine suggests that it increases glucose tolerance and does so in a way that is more effective than existing drugs.
Antidiabetic drugs currently on the market increase what's called the basal levels of insulin secretion—it goes up all the time, whether it's needed or not. This basal insulin secretion is a major cause of lethal hypoglycemia in the patients who take these drugs. New types of drugs that only boost insulin in response to glucose are thus highly desirable.
To do that, we need to be able to manipulate the pancreas. It's a somewhat unusual organ; many neural receptors are also found in pancreatic islet cells and, as of now, we don't really know what we are doing there. So some researchers in Europe decided they might be the key to tweaking the pancreas' activity.
In the brain, NMDA receptors are the ones targeted by DXM. To see what NMDA receptors are doing in pancreatic islet cells, these researchers took the tried and true approach of eliminating them and seeing what happened. The researchers removed the receptors genetically by knocking them out in mice. They also removed them pharmacologically, by treating mice with DXM and other molecules that block signaling through these receptors.
When the NMDA receptors were removed, either genetically or functionally, glucose-stimulated insulin secretion went up. Importantly, basal insulin secretion did not. DXM targets other receptors and neural tissues, so it could be acting indirectly, via the nervous system. To confirm that DXM enhanced glucose-stimulated insulin secretion by blocking the NMDA receptors in the islet cells, the researchers checked if DXM could achieve the same effect in islet cells from the NMDA knockout mice. It could not, confirming that it must in fact act through these receptors.