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Diazoxide Can Preserve Insulin Production in Type 1 Diabetes

Sep 14, 2004
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Early treatment of patients with type 1 diabetes with diazoxide, an inhibitor of insulin secretion, temporarily preserved residual insulin production in a recent study. Diazoxide (dye-az-OX-ide) Proglycem in the US when taken by mouth is used in the treatment of hypoglycemia (low blood sugar). It works by preventing release of insulin from the pancreas.

Dr. Eva Ortqvist, at Karolinska Hospital in Stockholm, and her team explain that, partial preservation of islet beta-cell function, by preserved insulin production, is associated with better glycemic control in children with the use of diazoxide.

 

Previous experiments have shown that diazoxide, an ATP-sensitive potassium channel opener, can protect beta-cells in vitro. In adults, the authors found that diazoxide increased residual insulin secretion.

In their current study, Dr. Ortqvist’s group randomly assigned patients newly diagnosed with type 1 diabetes to treatment with diazoxide 5 to 7.5 mg/kg in divided doses daily (n = 27) or to placebo (n = 29) for a total of 3 months. All participants were treated with multiple daily insulin injections.

Diazoxide partially suppressed endogenous insulin production, as demonstrated by decreases in basal and stimulated C-peptide concentrations by approximately 50% at 1 month and 30% at 3 months, compared with placebo.

After cessation of treatment, meal-stimulated C-peptide concentration was significantly higher at 12 months in the diazoxide group (p = 0.018), and tended to fall less by the end of the 24-month observation period.

Treatment had no effect on insulin requirements or long-term glycemic control, the investigators report. Side effects — excess hair growth, edema — were common.

"New ATP-sensitive K+ channel openers, with higher specificity and less side effects, added on to optimal insulin treatment with glucose control, or in combination with new immunosuppressive regimens, should be of interest for a further evaluation of the full potential of beta-cell rest to preserve residual insulin secretion in early type 1 diabetes," Dr. Ortqvist’s group concludes.
Diabetes Care 2004;27:2191-2197.

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