Moderate use averts failure of type 2 diabetes drugs in animal model
The drugs, sulfonylureas, help type 2 diabetics make more insulin, improving control of blood sugar levels. But in most patients the effects of sulfonylureas are lost after several years of use, causing insulin secretion to shut down. This typically forces patients to switch to regular insulin injections.
“Why this happens isn’t clear yet, but we’ve found what may be cause for hope,” says senior author Colin G. Nichols, Ph.D., the Carl F. Cori Professor and professor of cell biology and physiology. “We’ve shown in a mouse model that whatever causes this shutdown doesn’t kill the insulin-making beta cells of the pancreas or stop them from making insulin. Instead, it somehow stops them from secreting insulin.”
When they stopped receiving the drug, beta cells began secreting insulin again hours later. Nichols and co-author Maria Sara Remedi, Ph.D., instructor of cell biology and physiology, report the findings in Public Library of Science Medicine.
“I find these experimental observations very exciting,” says Alan Permutt, M.D., professor of medicine and of cell biology and physiology. “But I’m very cautious that patients understand that the relevance of this model to human diabetes and its treatment still needs to be tested.”
If human beta cells also survive and can continue to produce insulin after long-term sulfonylurea exposure, it may be possible to rethink treatment strategies, Nichols suggests.
“Doctors now prescribe new long-acting sulfonylureas to establish a chronic presence of the drug in the bloodstream,” he says. “But it may be beneficial to use the older drugs that go away more quickly, allowing the beta cells time to recover.”
Another potential option would be alternating periods of drug treatment with periods when the patient’s symptoms are managed by insulin injection, Nichols suggests.
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