Recent University research focusing on a particular gene in diabetes-prone mice may help pave the way for several practical, human applications regarding the Type 1 form of the disease.
According to Craig Nunemaker, director of the University's Pancreatic Islet & Cell Core Facility, researchers used a specifically bred non-obese mouse that was susceptible to developing a form of diabetes similar to the Type 1 variety.
Type 1 diabetes, according to University Microbiology Prof. Marcia McDuffie, who coauthored the research report with Endocrinology Department Chair Jerry Nadler, is an autoimmune disease in which a human body's white blood cells attack a subset of cells in the pancreas.
This immune system attack damages the cells to such a degree that they are no longer able to produce insulin, a hormone required for maintaining the regular transfer of glucose to other cells, McDuffie said.
In an attempt to further understand the disease -- which affects almost 3 million Americans -- Nunemaker said researchers "knocked out" a gene in the test mice known as 12/15-lipoxygenase. McDuffie explained this process involved "replacing a critical part of the gene's DNA sequence, so the body can never make a protein out of that gene."
The 12/15 gene, according to McDuffie, normally causes mice to produce an enzyme that seems to play a substantial role in activating the body's autoimmune attack.
In this case, McDuffie added, knocking out the 12/15 gene made the diabetes-prone mice incapable of getting the disease.
"The mice were slow to activate their white blood cells, and even when the cells did get to the pancreas ... they [couldn't] do damage," McDuffie said.
Nunemaker said only about two percent of the "knock-out" mice developed diabetes.
"One mouse ... out of 40," Nunemaker said. "We've really only had one case since I've been here."
McDuffie noted that the research has helped identify a "candidate gene." Future research focusing on this gene in other test subjects, she said, may help develop ways to predict whether a person is susceptible to diabetes and may aid in the development of a drug that could prevent the enzyme's possible activation of white blood cells.
"It shows there is a role for this particular gene in the progression of the disease, at least in mice," Nunemaker said.
Nunemaker and McDuffie added that no malignant side effects appeared in the mice after the 12/15 gene was turned off.
McDuffie noted, however, that research remains to be done in order to find a cure for diabetes.
"It's a solid finding," McDuffie said. "But we haven't cured anything yet."
Nunemaker noted that while the mouse model has proved in the past to be a reasonably reliable one, researchers cannot always use the same methods -- such as gene manipulation -- on human subjects.
"But much of what we know about the human disease we learned about in the mice," McDuffie said.
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