The term “‘Prion’ can be described as a mysterious infectious agent responsible for several neurodegenerative diseases in mammals, including Mad Cow Disease. Prions are a protein that protein is also implicated in diabetes, a recent study suggests.
Now here is the skinny, researchers stimulated diabetes from one mouse to another simply by injecting the animals with this protein. The results don’t indicate that diabetes is contagious like the flu and does not necessarily mean that a blood transfusion, or food and beverages, may spread the disease.
Researchers from McGovern Medical School at The University of Texas Health Science Center at Houston have detected symptoms of diabetes that can be triggered by a misfolded form of a pancreatic protein. The findings, reported in The Journal of Experimental Medicine notes the possibility that type 2 diabetes can be transmitted in the same way Creutzfeldt-Jakob disease or Bovine Spongiform Encephalopathy (mad cow disease) are passed from person to person.
The work is “very exciting” and “well-documented” for showing that the protein has some prion-like behavior, notes prion specialist Witold Surewicz of Case Western Reserve University in Cleveland, Ohio. However, he warns that it does not prove that diabetes can be spread from person to person. Although the science raises that possibility, he insists that “it remains to be determined.”
Prions are best described as misfolded proteins that can trigger healthy folded versions of the identical protein to misfold themselves. When such a conversion happens in the brain, the misfolded proteins clump together inside cells and destroy them. Although prion diseases are not common, they do share some characteristics with Huntington disease and other brain maladies.
Although initially, type 2 diabetes, doesn’t appear to have any connection to prions or neurodegenerative diseases. How the cells of the pancreas amass clumps of a protein known as islet amyloid polypeptide (IAPP), which is very similar to the β amyloid that accumulates in Alzheimer’s disease in people suffering from the type 2 version of the blood sugar disease. As a consequence, such protein deposits may eventually destroy many of the β cells in the pancreas that manufacture the hormone insulin.
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In the recent study, neurobiologist and biochemist Claudio Soto and his associates at the McGovern Medical School tested whether IAPP alone could trigger diabetes in mice. Scientists began culturing pancreatic cells from healthy humans and mice that had been genetically engineered to synthesize large quantities of human IAPP. The material, once added by researchers from the pancreases of old engineered mice that were already suffering from diabetes, the investigators noted how clumps of IAPP began growing in the cultured cells. The clumps, researchers noted, also manifest after the cells were exposed to lab-synthesized IAPP tangles.
Although rodents that had been genetically modified to crank out human IAPP were normally healthy, when scientists injected them with synthetic IAPP or with material from diabetic mice’s pancreas, IAPP conglomerations began to grow in the pancreases of the rodents. Just like prions, a tiny amount of misfolded IAPP behaves like a seed that roots, triggering new clumping of the abnormal protein to develop.
When scientists later tested whether inducing IAPP conglomerations in mice sparked the symptoms of type 2 diabetes, the data confirmed the possibility. Animals affected had higher blood glucose concentration than the control subjects. And just like their human counterparts with diabetes, the mice glucose tolerance texts were not only abnormal, large amounts of β cells died in their pancreases.
“We can induce the full-blown disease just by administering these protein aggregates” Soto notes. But he quickly conceded. “It’s not like the flu.” But he thinks more investigation is required to determine whether diabetes can be transmitted as a consequence of blood transfusions or organ transplants.
