Aim: To study the impact of intensified therapy with the dipeptidyl peptidase-4 (DPP-4) inhibitor vilagliptin or sulfonylurea (SU) on the control of glycemia, weight, and quantitative body composition in patients with type 2 diabetes mellitus (DM-2) who have failed to achieve compensation during metformin monotherapy.
Subjects and methods: Forty patients (mean age 55.0 (range 53.0-60.7) years; disease duration 2.0 (range 1.1-5.0) years) with poor glycemic control (7%<HbA1c <10%) during metformin monotherapy were allocated to 2 groups for 6-month therapy. In group 1 (n=20), vildagliptin 100 mg/day was added to metformin; in Group 2 (n=20), the latter was added by SU with its dose adjustment. Dual-energy X-ray absorptiometry was used to quantify body composition at baseline and after 6 months. The efficiency of glycemic control and adiponectin level changes was evaluated at baseline and after 3 and 6 months.
Results: Following 6 months of treatment, both groups achieved a comparable reduction in HbA1c levels; however, the number of glycemic episodes during SU treatment was found to be significantly higher. When vildagliptin was used in combination therapy, with the lean body mass being preserved, there was a statistically significant decrease in total body weight, body mass index (BMI), fat mass, and tissue fat percentage without considering bone mass, as well as waist circumference (WC), which was attended by an elevation of adiponectin levels. On the contrary, when SU therapy was intensified, total body weight, fat mass, BMI, and WC were statistically significantly increased and adiponectin levels remained unchanged.
Conclusion: The glucose-lowering efficiency of combination therapy with metformin + vildagliptin, a DPP-4 inhibitor, was comparable with that of a metformin + SU combination, but safer with respect to the risk of developing hypoglycemia. Addition of vildaglptin to metformin monotherapy may cause an additional favorable effect in reducing body weight at the expense of a fat component, with the lean body mass being preserved, and in elevating the level of adiponectin, an adipose tissue-derived antiatherogenic hormone.