Fighting Back Against Diabetes

Psoriasis medication could be the key to a new kind of diabetes treatment

Type 1 diabetes causes certain cells in the body to destroy insulin-producing cells, so patients must control their blood sugar with insulin therapy. But what if a medicine could launch a counterattack on the harmful cells?

Recent research looked at a possible new treatment for type 1 diabetes that targeted the cells that attack the pancreas. The drug they used is normally prescribed to treat a skin disorder, but the researchers administered it to patients with type 1 diabetes.
They found that the participants showed some improvement in insulin production, meaning that the new treatment was somewhat effective.
The research could be used to develop new ways of treating type 1 diabetes, which would reduce patients' reliance on insulin therapy.

"Talk to your doctor about possible treatment options if you have type 1 diabetes."

Mark Rigby of Indiana University and the Riley Hospital for Children in Indianapolis, Indiana led the study in order to see if the drug alefacept could help treat type 1 diabetes.
Type 1 diabetes is a disease in which the body destroys cells in the pancreas that produce insulin. Insulin is a hormone that regulates blood sugar levels in your body. Without enough insulin, a diabetes patient experiences high blood sugar. Type 1 diabetes is different from type 2 diabetes, which is when the body loses sensitivity to insulin. 
Without proper treatment, type 1 diabetes can be very dangerous and lead to a coma and possibly death. Typically, type 1 diabetes is treated with insulin supplements.
Previous studies have explored whether there are alternate treatments to type 1 diabetes that involve stopping the destruction of insulin-producing pancreas cells. This recent study tested that theory with the drug alefacept.
Alefacept is typically used to treat psoriasis, a skin disorder. Alefacept works by attacking two types of cells, the same cells that destroy pancreatic cells which produce insulin. The researchers thought that the medicine might be effective in treating type 1 diabetes and stabilizing insulin production.
They tested their theory in a controlled trial using 49 type 1 diabetes patients. Each of the patients had been diagnosed in the previous 100 days and were between 12 and 35 years old.
Of the participants, 33 received alefacept and 16 received a placebo, or fake medication. The group that received alefacept received 15 mg of the drug every week for 12 weeks, then took 12 weeks off, and then received the same 12-week regimen as before.
After the patients had received the full treatment, they were screened and had their blood taken. The researchers measured the amount of insulin that the pancreas produced in the two hours and four hours after the participants ate food.
The primary outcome that the researchers looked for was an increase in insulin production two hours after eating. However, for both the alefacept and placebo groups, insulin production remained about the same.
After four hours, however, the group that had received alefacept had significantly increased preserved insulin secretion, while the placebo group's insulin production had dropped off.
Additionally, one year after the beginning of treatment, the participants in the alefacept group were using less supplementary insulin than the placebo group. The treatment group also experienced far fewer events of dangerously low blood sugar resulting from an insulin shot.
According to the researchers, these outcomes mean that the alefacept was able to target the destructive cells in order to preserve the patients' pancreatic cells. 
The results of the study could lead to new kinds of medical treatment for type 1 diabetes, the study authors wrote, but larger trials would need to be done to target the harmful cells while preserving beneficial cells.
This study was published in The Lancet Diabetes & Endocrinology on September 22.
The research was funded by the US National Institutes of Health and the Juvenile Diabetes Research Foundation. One of the authors reported receiving research funds, but the other authors declared no conflicts of interest.
Review Date: 
September 20, 2013