More than 30 children who appeared to have type-1 diabetes were weaned off insulin by a clever application of modern genetics and the tweaking of ion channels.
All these children suffered from permanent neonatal diabetes. They had a genetic mutation that, by altering the function of a potassium channel involved in glucose sensing, mimics insulin-dependent diabetes. The damage caused by the mutation can be repaired by giving the children a common, inexpensive, oral drug used to treat type-2 diabetes.
The developer of this therapy is an English physician named Andrew Hattersley, of Peninsula University. He has focused on these genetically triggered versions of diabetes since 2004. But until recently this approach never gained much attention in the US.
An interesting sidelight is that by genetic testing of children with very early onset diabetes, the team has found several other diabetes-causing mutations, although so far no immediately treatable ones. Some have tiny alterations of their insulin genes. Other forms of monogenic diabetes that can masquerade as either type-1 or type-2, some of them discovered at the University of Chicago, also remain under-diagnosed.