Novel diabetes strain has rapid onset
By Nathan Seppa
Every year, thousands of people, young and old, experience the malaise and nagging thirst that are characteristic of untreated type I diabetes. Also called juvenile-onset diabetes, this disease stems from the death of beta cells in the pancreas. These cells make insulin, the hormone that regulates sugar metabolism. In most patients, their own immune cells do the killing.
Japanese scientists have now confirmed that some patients have a peculiar kind of diabetes that doesn’t fit this pattern. Instead of immune cells, an unknown agent—possibly a virus or a chemical in the environment—seems to destroy the beta cells. Moreover, these patients fall ill rapidly, the researchers report in the Feb. 3 New England Journal Of Medicine.
“We all have patients where we sometimes wonder what happened,” says physician David C.W. Lau of the University of Calgary in Alberta. This study establishes “an important subtype of type I diabetes that is different from the conventional diabetes that we associate with children. . . . Diabetes is more complex than we previously thought.”
In most cases, physicians can ascertain that a patient has type I diabetes by gauging symptoms and testing for diabetes-related antibodies in the blood, a sure sign of an immune attack on the pancreas. However, of 56 randomly selected Japanese patients newly diagnosed with the disease, 11 had no trace of such autoimmune antibodies but still showed high sugar concentrations in the blood and other pancreatic abnormalities.
Researchers took pancreas tissue samples from three of these patients. Examination showed no immune-cell invasion of the cell clusters that harbor beta cells. Tests on tissue from three of the patients with conventional type I diabetes revealed the expected immune attack.
Furthermore, the 11 patients, aged 25 to 57, had had symptoms for an average of only 4 days before their condition drove them to see a physician, who diagnosed full-blown diabetes, says coauthor Akihisa Imagawa, an endocrinologist at Osaka University. In the other patients, the onset took about 50 days.
The cause of this subtype of diabetes is unclear. “Some unknown pathogen . . . attacked the pancreatic beta cells,” Imagawa says. Patients with the novel subtype of diabetes showed signs that the pancreas as a whole was affected, not simply the beta cells. That may be evidence of a viral infection, Imagawa says.
Past studies have hinted at a link between viruses and diabetes but haven’t provided solid proof.
The pancreas damage could also arise from an environmental factor, says Ake Lernmark, an endocrinologist at the University of Washington in Seattle. Chemicals called nitrosamines, which can derive from nitrates such as those in smoked meats and other cured foods, have been weakly associated with increased diabetes incidence, he says.
The new study “will boost research to find environmental factors that might actually be causing diabetes,” Lernmark says.