A new study reveals the molecular basis of chronic nerve pain in diabetes, which could lead to new treatments that target the source of this type of pain. Researchers from King’s College London published their findings in Science Translational Medicine,
About one-fourth of people with diabetes develop painful diabetic neuropathy (PDN), which is a chronic pain condition often described as sharp, shooting pains and extreme sensitivity to touch in the feet and hands. If can significantly impair mobility and is very difficult to treat.
The molecular causes PDN are poorly understood. This new study provides evidence that a single protein molecule – HCN2 – can by itself be responsible for a complex sensation such as diabetic pain.
The researchers used mouse models of diabetes to show that over-activity of HCN2, which initiates electrical signals in pain-sensitive nerve fibers, results in a sensation of pain. They also found that blocking the activity of HCN2, or removing it completely from pain-sensitive nerve fibers, stopped the sensation of pain entirely.
Professor Peter McNaughton, who is the senior author of the studysaid, “The inexorable rise of obesity worldwide, in both rich and poorer countries, has brought a related increase in type 2 diabetes. As many as one in four diabetics suffer from nerve pain, yet there are currently no effective treatments and people therefore typically must resign themselves to a life of continuous suffering.”
“Our study reveals the molecular mechanism driving diabetic pain in mice, which we hope will inform future treatments in people with diabetes,” he added
Dr. Christoforos Tsantoulas, first author of the study, said, “At present we do not have selective drugs which can suppress the activity of HCN2 without affecting other bodily functions, such as the regulation of heart rate. This research provides a stimulus for the development of targeted pain drugs that can block HCN2 without affecting the activity of other molecules.”