Read more

August 02, 2016
2 min read
Save

Short-term intensive insulin therapy may induce type 2 diabetes remission

In patients with type 2 diabetes, short-term intensive insulin therapy, especially within 2 years of diagnosis, may induce diabetes remission without requiring other antidiabetes medications, study data show.

“There is a window of opportunity within the first years of diagnosis of [type 2 diabetes] during which intervention with short-term [intensive insulin therapy] can preserve beta-cell function and induce sustained drug-free remission of diabetes,” Ravi Retnakaran, MD, FRCPC, clinician-scientist and endocrinologist at Leadership Sinai Centre for Diabetes and Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital (Toronto) and associate professor in the department of medicine at the University of Toronto, told Endocrine Today. “The key clinical implication is that intervention with short-term [intensive insulin therapy] to try to preserve beta-cell function and change the natural history of [type 2 diabetes] should ideally be implemented within the first 2 years of [type 2 diabetes].”

Ravi Retnakaran

Ravi Retnakaran

Retnakaran and colleagues evaluated 25 adults with early type 2 diabetes ( 7 years’ duration) who underwent 4 weeks of intensive insulin therapy (multiple daily injections of basal insulin detemir and prandial insulin aspart) followed by placebo for 48 weeks to determine whether short-term intensive insulin therapy can induce remission that remains during the placebo period.

Every 12 weeks, participants underwent an oral glucose tolerance test to allow for serial assessment of insulin sensitivity, alpha-cell response and beta-cell function. Remission was defined as HbA1c less than 6.5% without medication for type 2 diabetes.

At 48 weeks after intensive insulin therapy, 56% of participants were in drug-free remission . At baseline, the remission group had a shorter duration of diabetes (P = .03), lower HbA1c (P = .006) and better beta-cell function measured by Insulin Secretion-Sensitivity Index-2 (P = .01) compared with the non-remission group.

Compared with the non-remission group, the remission group had lower doses of basal insulin (P = .002) and meal insulin (P = .01) during intensive insulin therapy. One day after intensive insulin therapy, the remission group had lower levels of HbA1c and better beta-cell function compared with the non-remission group; however, the differences were not as pronounced as they were at baseline. Differences in HbA1c (P < .001) and Insulin Secretion-Sensitivity Index-2 (P < .001) were more apparent between the two groups after 48 weeks.

Shorter duration of diabetes was a better independent predictor of remission compared with baseline HbA1c and beta-cell function. Persistence of remission was predicted by diabetes duration less than 2 years.

“Short-term intensive insulin therapy, for 4 weeks, can induce a sustained drug-free remission of type 2 diabetes that persists for 48 weeks after stopping the insulin,” Retnakaran told Endocrine Today. “Although short-term intensive insulin therapy is known to have beneficial effects on insulin resistance, glucagon regulation and beta-cell function, the effects on insulin resistance and glucagon are not sustained indefinitely after stopping the insulin. In contrast, the patients who experience sustained drug-free remission show a long-term preservation of beta-cell function after [intensive insulin therapy] that is likely the basis for the remission. However, the key determinant of the likelihood of inducing sustained remission with short-term [intensive insulin therapy] is early intervention, particularly within the first 2 years after diagnosis of diabetes. – by Amber Cox

For more information:

Ravi Retnakaran , MD, FRCPC, can be reached at Leadership Sinai Centre for Diabetes, Mount SInai Hospital, 60 Murray Street, Suite L5-025, Mailbox 21, Toronto, Ontario, Canada M5T 3L9; email: rretnakaran@mtsinai.on.ca.

Disclosure: Retnakaran reports having received funding from Novo Nordisk. Please see the full study for a list of all other authors’ financial disclosures.