New York: A drug currently used in Europe and Asia for treating gallstone-related spasms has been found effective in preventing the onset of Type-1 diabetes in mice, according to a study.
Researchers believe that a similar treatment may be effective in preventing the autoimmune disorder in humans too.
The study found that the buildup of a substance in the pancreas during the pre-symptomatic stage of Type-1 diabetes is essential to the development of the disease.
Administering a drug to block production of this substance stops damage to insulin-producing cells and prevents the onset of the autoimmune disorder, the findings showed.
The researchers earlier found that one substance, called hyaluronan, was overly abundant near the pancreatic beta cells of people with Type 1 diabetes.
"We wondered what would happen if we prevented that buildup," said the study's senior author Paul Bollyky, assistant professor of infectious diseases at Stanford University School of Medicine in California, US.
"And we knew a drug that does that," Bollyky noted.
The drug was hymecromone, or 4-methylumbelliferone (4-MU for short).
When the researchers initiated 4-MU treatment before the majority of the mice's beta cells had been wiped out, none of the mice developed excess glucose in their bloodstream.
Mice that did not get 4-MU did. If mice stayed on a 4-MU regimen, they remained diabetes-free for at least a year.
But if the regimen was stopped, they quickly became diabetic.
The researchers said they are now preparing for human trial to test the effectiveness of 4-MU in preventing Type-1 diabetes.
The study was published in the Journal of Clinical Investigation.
Researchers believe that a similar treatment may be effective in preventing the autoimmune disorder in humans too.
The study found that the buildup of a substance in the pancreas during the pre-symptomatic stage of Type-1 diabetes is essential to the development of the disease.
The researchers earlier found that one substance, called hyaluronan, was overly abundant near the pancreatic beta cells of people with Type 1 diabetes.
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"And we knew a drug that does that," Bollyky noted.
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When the researchers initiated 4-MU treatment before the majority of the mice's beta cells had been wiped out, none of the mice developed excess glucose in their bloodstream.
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But if the regimen was stopped, they quickly became diabetic.
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The study was published in the Journal of Clinical Investigation.
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