Influence of IDPP-4 on Fat Metabolism in Patients with Type 2 Diabetes

Abstract

According to IDF, more than 425 million people in the age of 20 to 79 all around the world are suffering from type 2 diabetes. In 2045, the number of people will reach 629 million. Such a rapid increase in the prevalence of type 2 diabetes is associated with increasing of patients with obesity. A whole range of mechanisms involving many organs and hormonal systems supports glucose homeostasis, and dysfunction of this systems leads to the development and progression of insulin resistance and the development of complications. Early start of therapy that aimed at the maximum number of pathophysiological targets can slow the progression of disease and prevent. The purpose of our study is to evaluate the influence of combined therapy of sitagliptin and metformin on fat metabolism in patients with type 2 diabetes mellitus. The study included 82 patients (age, 55.3±9.1 years) with obesity and lipid metabolism disorders. None of the patients had reached their target glycated hemoglobin levels after metformin and diet therapy. Patients in group 1 (n=42) received 1.5–2-g metformin daily before the study and were switched to a formulation of 100-mg sitagliptin and 2-g metformin once a day. Patients in group 2 (n=40) were on a diet therapy before inclusion and were started on 2-g metformin/day. The following were evaluated at baseline and after 6 months of therapy: fasting glucose levels, postprandial glucose levels, glycated hemoglobin, weight, body mass index, waist circumference and lipid profile; insulin, proinsulin, leptin and adiponectin levels; insulin resistance using the homeostatic model assessment (HOMA) of β-cell function (HOMA-β) and insulin resistance (HOMA-IR). In addition, magnetic resonance imaging was performed to assess the amount of visceral fat for the total cohort. As the result of intensification of therapy by adding sitagliptin to metformin, in patients with type 2 diabetes, compared to monotherapy with metformin, we got more pronounced important non – glycemic effects in the form of a decrease in the visceral fat depot, an improvement in functional activity of pancreatic β-cells, which is the leading pathogenesis mechanism for improving glycemic control.