Type 1 diabetes was previously thought to render the pancreas completely unable to produce insulin, the hormone responsible for controlling sugar entry into cells and subsequent blood levels.
The truth, researchers have now discovered, is that very small amounts of insulin are produced in "most" patients, and that levels in the blood even respond to food intake.
The early-onset form of diabetes was thought to kill off all the specialized insulin-secreting beta cells in the pancreas within a few years of developing the condition.
Or, as the study authors put it: "Type 1 diabetes is defined as a disease of progressive autoimmune destruction of beta cells, leading to absolute insulin deficiency."
But their new finding, published in Diabetologia, the journal of the European Association for the Study of Diabetes, shows that some beta cells are either resisting the immune attack that causes people with type 1 diabetes to lose these specialized cells, or they are regenerating themselves.
The development has been enabled by new technology that can measure very small concentrations of insulin in the blood, and the revelation that not all beta cells are killed raises the prospect of treatments that halt or reverse the autoimmune damage in type 1 diabetes.
Until such options are developed, people with type 1 diabetes, who are usually diagnosed in their teens, must rely on daily injections of insulin to keep their blood sugars under control.
The new research was led by the UK's University of Exeter Medical School and funded by the charity Diabetes UK.
It found that around three-quarters of patients with the condition possess a small number of beta cells that are not only producing insulin, but also doing so in response to food, "a sign that the cells are healthy and active."
The authors conclude: "This implies that beta cells are either escaping immune attack or undergoing regeneration."
The scientists found that 73% of the volunteers (54 out of 74) in the study produced low levels of insulin, regardless of the length of time since their diagnosis.
New technology detects tiny concentrations
The response of the insulin production to a meal proved that the low-level production was coming from working beta cells, the researchers say. The levels of insulin were so low that without this response to food, the effect could have been ascribed to "analytical noise."
Insulin levels were detected in the study by testing for a blood marker of the hormone called C-peptide.
Scientists were previously able to measure levels of this substance only at blood concentrations above 30 pmol/l - whereas the new "ultrasensitive assays" are able to detect levels ten times smaller, down to 3.3 pmol/l.
"The impact of using a modern assay with a lower limit of detection is more apparent with increasing disease duration," the authors say, so that 68% of the volunteers who had lived with their diabetes for over 30 years showed levels of insulin that would have been hidden previously, when a proportion of just 11% of participants would have shown working beta cells.
Dr. Richard Oram, of the University of Exeter Medical School, who led the study, says: "The researchers used new technologies which are able to detect far lower levels of insulin than was previously possible. The levels are so low that scientists had previously thought no insulin was produced."
Dr. Oram continues:
"It's extremely interesting that low levels of insulin are produced in most people with type 1 diabetes, even if they've had it for 50 years.
The fact that insulin levels go up after a meal indicates these remaining beta cells can respond to a meal in the normal way - it seems they are either immune to attack, or they are regenerating."
Diabetes UK's head of research, Dr. Matthew Hobbs, says there has been a lot of research into ways of making new beta cells that can be transplanted into the body. This is driven by the fact that "preserving or restoring even relatively small levels of insulin secretion" in type 1 diabetes can prevent the low glucose levels of hypoglycemia and reduce complications.
Dr. Hobbs adds:
"This research shows that some of a person's own beta cells remain and therefore it may be possible to regenerate these cells in the future.
It is also possible that understanding why some people keep insulin production whilst others lose it may help answer key questions about the biology of type 1 diabetes and help advance us towards a cure for the disease."
Hope that type 1 diabetes is not an insulin 'write off'
The next step is a larger-scale study, Dr. Oram says, to help understand the genetics and immune systems of people with type 1 diabetes who are still making insulin. The research would also help answer "the important question" of whether these people have fewer complications.
Developments in this area would mean a lot to people like Alex Nesbitt, one of the participants in the present study. He is 56 years of age and was diagnosed with type 1 diabetes when he was 20. He is monitored by an insulin pump that is permanently attached to his body.
He says the condition has been "trying in the extreme," with a stigma attached to it. "For a very long time," he says, "people have believed that if you have type 1 diabetes, that's the end of your insulin production."
"This study raises some major questions about whether that's actually the case. It's very exciting for current opinion to be challenged in this way, and I'm fascinated to know what difference it will mean for the future."Written by Markus MacGill