October 7, 2011
Diabetes Susceptibility Gene Found After Years Of Effort
Researchers from the University of Wisconsin—Madison have discovered the specific gene that gives diabetes susceptibility to obese mice. The study, published in the journal PLoS Genetics, shows that the protein tomosyn-2 can act to modulate insulin secretion from the pancreas.
The researchers focused on tomosyn-2 while searching for gene snippets contributing to diabetes susceptibility in obese animals.Alan Attie, a UW—Madison biochemistry professor and lead researcher says, “It´s too early for us to know how relevant this gene will be to human diabetes. But the concept of negative regulation is one of the most interesting things to come out of this study and that very likely applies to humans.”
When working correctly insulin is secreted into the blood after eating which helps maintain blood sugar at a safe level. Type 1 and type 2 diabetes both lead to high blood sugar and diabetic symptoms.
Blood glucose levels, caused by too much insulin, becomes dangerously low and lead to coma or even death. The scientists found tomosyn-2 while searching for genes that contribute to diabetes susceptibility in obese lab mice.
Genetic analyses and comparisons of obese diabetes-resistant and diabetes-susceptible mouse strains revealed a single amino acid difference that destabilizes the tomosyn-2 protein in the diabetes-resistant mice, effectively releasing the brake on insulin secretion and allowing those animals to release enough insulin to avoid diabetes.
Diabetes is highly unlikely to be caused by a single gene, it is believed. Identifying important biological pathways can suggest clinically useful targets. “This study shows the power of genetics to discover new mechanisms for a complex disease like type 2 diabetes,” says postdoctoral fellow Sushant Bhatnagar, a co-lead author of the paper.
“Now we know there are proteins that are negative regulators of insulin secretion. Very likely they do the same thing in human beta cells, and it motivates us to move forward to try to figure out the mechanisms behind that negative regulation,” Attie says.
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