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Early Intensive Therapy in Type 2 Diabetes Preserves Beta-Cell Function

August 2012, Vol 5, No 5, Special Issue ADA 2012 Highlights

Intensive therapy initiated in newly diagnosed patients with type 2 diabetes can preserve beta-cell function, according to data released by Ildiko Lingvay, MD, Assistant Professor of Internal Medicine at the University of Texas Southwestern Medical Center, Dallas, at the 2012 ADA annual meeting.

Progression of type 2 diabetes hinges on a progressive decline in beta-cell function over time, and Dr Lingvay recommended that “we try to achieve glycemic normalization as quickly as possible after diagnosis. In addition, I recommend we maintain glycemic control long-term.”

Dr Lingvay and colleagues sought to study the effects of a treatment strategy they devised, with the intent of preserving beta-cell function. The study started with a run-in period of 3 months in which 63 newly diagnosed, treatment-naive patients aged 21 to 70 years were treated with insulin (70/30 aspart premix) and metformin (500 mg daily, which was titrated weekly to 1000 mg twice daily). The run-in period was designed to remove any preexisting glucotoxicity and associated temporary beta-cell stunning.

Patients were then randomized to either continuation of insulin and metformin or to triple oral therapy—glyburide 1.25 mg twice daily, which was titrated throughout the study; metformin 1000 mg twice daily; and pioglitazone 15 mg daily, titrated monthly to a final dosage of 45 mg daily). A total of 58 patients finished the 3-month run-in and were randomized.

A mixed-meal challenge test was used to assess beta-cell function at randomization and at 6, 12, 18, 30, and 42 months.

Treatment failure was predefined as a hemoglobin (Hb) A1c level >8%. If patients in the triple oral arm achieved this target, they were transitioned to insulin and metformin. Those assigned to the insulin group who achieved this target remained on insulin, with the option to change the frequency or type of treatment.

Treatment failure occurred in 3 patients in the insulin group and 5 patients in the triple oral therapy group.

At the time of diagnosis, the average HbA1c was 10.6%. After the 3-month run-in period, the HbA1c was reduced to 5.9% and all participants achieved an HbA1c level <7%.

After 3.5 years, 83% of patients receiving insulin plus metformin and 72% of those receiving triple oral therapy had completed the study.

Beta-cell function was preserved in both groups, with no significant change over time in beta-cell function between or within groups, as calculated by C-peptide area under the curve (AUC) or glucose AUC, said Dr Lingvay.

There was an increase in body weight in both groups, with no significant difference between groups.

Mild hypoglycemia, defined as home glucose measurement of <70 mg/dL associated with any symptoms suggestive of hypoglycemia, occurred at a rate of 1 monthly during the first 4 months. The rate decreased significantly over time, to <0.5 events monthly by the end of the study, and did not differ significantly between groups.

“This is a very important finding, in light of a very low HbA1c achieved and maintained throughout the study,” noted Dr Lingvay.

Because diabetes is a multifactorial disease, monotherapy may not be adequate to change the course of the disease, she pointed out. “I recommend combination treatment with complementary mechanisms of action….Treatment intensification should be done while the patient’s glycemic control is still within the target range. I would not recommend waiting until HbA1c goes above target before intensifying treatment.”

Because of the design of the study, it is not known whether the beta-cell preservation effect could be attributed to the initial insulin-based therapy during the run-in phase or to the ongoing therapy received after randomization, Dr Lingvay noted.

Last modified: August 30, 2021