A new study by 'King's College' in London, in the United Kingdom, reveals the molecular base of chronic nervous pain in diabetes.The findings in mice, published on Wednesday in the magazine 'Science Translational Medicine', could one day lead to treatments that point to the source of pain.
Around one in four people with diabetes develop a chronic pain -induced pain disease, called painful diabetic neuropathy (PDN), due to the high level of blood sugar.Symptoms include tingling and tingling sensations, as well as acute and sharp pains and extreme sensitivity to the foot and hands, which can extend up on the legs and arms.
Pain can significantly deteriorate mobility, which in turn exacerbates obesity and worsens type 2 diabetes in a self-perpetuation cycle.Diabetic pain is very difficult to treat and little is known about molecular causes.This new King's College study provides the first evidence that a single protein molecule-HCN2-can alone be responsible for a complex sensation such as diabetic pain.
The scientists used diabetes mouse models to demonstrate that the overactivity of HCN2, which begins electrical signals in pain -sensitive nerve fibers, results in a sensation of pain.They also found that the blockade of the HCN2 activity, or the complete elimination of pain -sensitive nerve fibers stopped the sensation of pain completely.
Professor Peter McNaughton, lead author of the study, of the Wolfson Center for age -related diseases at the King's College in London, says: "The inexorable increase in obesity worldwide, both in rich and richest countries, has led to an increase in type 2 diabetes. One in four diabetics suffers from nerve pain, however, there are currently no effective treatments and people, therefore, must be resigned to a life of continuous suffering. "
"Our study reveals the molecular mechanism that drives diabetic pain in mice, which we hope to provide information for future treatments in people with diabetes," he says.For his part, Dr. Christoforos Tsantoulas, first author of the study, also of the Wolfson Center for Age -related diseases at the King's College in London, says: "We currently have no selective drugs that can suppress the HCN2 activity without affectingOther bodily functions, such as heart rate regulation.
