A protein that may play a crucial role in the development of diabetes has been identified by scientists from University of Chicago.
A cellular protein from a family involved in several human diseases appears to play a role in proper production and release of insulin.
Lead researchers Deborah Nelson and Louis Philipson showed that mice lacking the ClC-3 channel, a passageway that allows negatively-charged chloride ions to pass through cell membranes, have only one-fifth the circulating insulin of normal mice.
They hope that the finding may explain a portion of what goes wrong in Type 2 diabetes and could help doctors find rare patients whose diabetes has a previously-undetected genetic origin.
"Chloride regulation is not really well understood, but it's at the heart of cystic fibrosis, and it is related to the regulation of how insulin gets made," said Philipson, professor of medicine and medical director of the Kovler Diabetes Center at the University of Chicago.
"Now we see that it's a critical feature of how insulin gets converted from a precursor form to its most active form."
A team lead by Ludmila Deriy, a research assistant professor in Nelson's laboratory, studied genetic knockout mice missing the ClC-3 chloride channel.
The blood of those mice contained lower levels of insulin. Missing ClC-3 therefore appears to cause a dramatic slowdown of the conversion of proinsulin to insulin.
A mutation in the function of ClC-3 in humans could very well be the cause of a select few cases of juvenile diabetes, Nelson and Philipson said.
The research is published in the journal Cell Metabolism.