Abstract
The ß-cell dysfunction of type 2 diabetes is partly reversible. The optimal time window to induce glycemic remission is uncertain; short courses of insulin treatment have been tested as a strategy to induce remission. In a pilot study in 38 newly-diagnosed patients, we assessed the time-course of insulin sensitivity and ß-cell function (by repeat oral glucose tolerance tests) following a 6-week basal insulin treatment compared to metformin monotherapy in equipoised glycemic control. At 6 weeks, insulin secretion and sensitivity were increased in both groups whilst ß-cell glucose sensitivity was unchanged. From this time onwards, in the insulin group glycemia started to rise at 3 months, and was no longer different from baseline at 1 year. The initial improvement in insulin secretion and sensitivity dissipated. In the metformin group, fasting plasma glucose and HbA1c levels reached a nadir at 8 months, at which time insulin secretion, glucose and insulin sensitivity were significantly better than at baseline and higher than in the insulin group. A short course of basal insulin in newly-diagnosed patients does not appear to offer clinical advantage over recommended initiation with metformin.
Highlights
There is ample evidence that the ß-cell dysfunction that defines type 2 diabetes can be, at least in part, reversed, leading to clinical remission in an interesting fraction of patients [1]
With regard to the mechanisms of insulin-induced diabetes remission, the focus appears to be on the ability of insulin to improve insulin secretion, in post-bariatric patients insulin resistance abates as a result of the large weight loss [5]
We were interested in examining the time trajectory of the principal pathogenetic mechanisms—namely, ß-cell function and insulin sensitivity—underlying the glycemic improvement that a short course of insulin can induce in newly-diagnosed patients
Summary
There is ample evidence that the ß-cell dysfunction that defines type 2 diabetes can be, at least in part, reversed, leading to clinical remission in an interesting fraction of patients [1]. We were interested in examining the time trajectory of the principal pathogenetic mechanisms—namely, ß-cell function and insulin sensitivity—underlying the glycemic improvement that a short course of insulin can induce in newly-diagnosed patients.
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