Canadian Researchers Show a Lot of Nerve

Nervous System Abnormality May Cause Type 1 Diabetes

Jan 25, 2007

The conventional wisdom that autoimmune dysfunction is solely responsible for type 1 diabetes may go up in smoke after the discovery by Canadian researchers that abnormal nerve endings are critical in the cause and cure of type 1 diabetes in mice. In the December 15 issue of Cell, Dr. Michael Dosch and his team reported that eliminating malfunctioning sensory nerve cells in the pancreas of NOD mice (Non-Obese Diabetic mice, genetically predestined to develop diabetes) prevented the disease; equally surprising, inserting a protein produced by healthy nerve cells into already diabetic mice cured them of diabetes within a single day.

The discoveries were so unexpected that they stunned the researchers themselves and sent a shock wave throughout the search-for-a-cure world. "I couldn't believe it," said Dr. Michael Salter, Dr. Dosch’s colleague at the Canadian Hospital for Sick Children, describing what happened when the pancreas of a diabetic mouse was injected with protein produced by healthy sensory nerves. "Mice with diabetes suddenly didn't have diabetes any more." Some mice, after just one injection, have remained diabetes free for as long as four months.

The researchers have not yet confirmed their findings in humans, but expect to do so within a year. They believe that nerve abnormalities will soon be implicated in many other diseases, including type 2 diabetes (they’ve already found this to be the case) and inflammatory ailments such as Crohn’s and asthma.

Dr. Dosch was led to his discovery when he noted that around the insulin-producing pancreatic islets were an "enormous" number of pain-signaling nerves, the type that tell the brain when tissue has been damaged. Suspecting a link between those nerves and diabetes, he and Dr. Salter killed the nerves in NOD mice that were genetically programmed to develop type 1 diabetes. "Then we had the biggest shock of our lives," Dr. Dosch said. Almost immediately, the islets began producing insulin normally.

The researchers, who included participants from the University of Calgary and the Jackson Laboratory in Maine, learned that the nerve cells secrete a protein (also called a neuropeptide) that is instrumental in the proper functioning of the islets. The nerve cells of NOD mice don’t secrete enough of the neuropeptide, called “substance P,” to sustain normal islet function. This causes inflammation around the islets and leads to their eventual destruction, resulting in type 1 diabetes in the mice. When the researchers injected "substance P" into the pancreases of already diabetic mice, the islet inflammation cleared up almost immediately, and the diabetes was gone.

The scientists believe that by secreting some, but not enough, “substance P,” the nerve cells initiate and sustain the cycle of inflammation and autoimmune responses culminating in type 1 diabetes. Consequently, either adding more “substance P” or removing the neural circuit altogether essentially eliminates the disease in mice. If this mechanism proves valid in humans, the implications for new cure-related research are hopeful.

Sources: Juvenile Diabetes Research Foundation; University of Calgary

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