Abstract
Background: There are few clinical trials addressing the difference in pleiotropic effects among dipeptidyl peptidase (DPP)-4 inhibitors. We aimed to identify difference in effects on biochemical markers of inflammation, oxidative stress, and atherosclerosis between two DPP-4 inhibitors in patients with type 2 diabetes. Methods: We prospectively observed twenty subjects with type 2 diabetes before and after a practical medication change from a treatment with pioglitazone and sitagliptin 50 mg to a combination tablet containing the same dose of pioglitazone and alogliptin 25mg, which was actually identical to switching from sitagliptin to alogliptin. After 3 months, changes from baseline in clinical data and various biochemical markers were evaluated. In particular, body mass index (BMI) and hemoglobin A1c (HbA1c) were additionally followed after 12 months for evaluation of chronic outcomes. Results: Among markers, serum levels of high molecular weight (HMW) adiponectin significantly increased from 6.9 ± 3.6 μg/ml to 8.2 ± 4.0 μg/ml (P = 0.0045). Although no clinical data changed after 3 months, significant improvements in HbA1c and BMI were observed after 12 months. Their rates of changes tended to inversely correlate with the increased percentages of serum HMW adiponectin levels during initial 3 months, but they did not reach statistical significance. Conclusions: In spite of pretreatment with pioglitazone, additional increase in serum HMW adiponectin levels was demonstrated after switching from sitagliptin to alogliptin. Given multiple favorable roles of adiponectin in metabolic and cardiovascular states, alogliptin, at least when combined with pioglitazone, would be beneficial in treatment of type 2 diabetes.
Highlights
Metabolic syndrome, which is characterized by visceral adiposity, is widely recognized as a risk factor for diverse metabolic disorders including type 2 diabetes, hypertension, and dyslipidemia, and causes atherosclerotic diseases
A total of 20 subjects were enrolled in the current study, and none of them withdrew over the 12-month observation period, indicating that there were no adverse events caused by just switching of dipeptidyl peptidase (DPP)-4 inhibitor from one to another
None of the other biochemical markers including monocyte chemoattractant protein (MCP)-1, highly sensitive C-reactive protein (Hs-CRP), total reactive oxygen species (ROS), oxidized-low density lipoprotein (LDL) cholesterol, asymmetric dimethylarginine (ADMA), or E-selectin changed (Table 2). These findings indicate that serum high molecular weight (HMW) adiponectin levels might increase through the mechanisms independent of inflammation, oxidative stress, atherosclerotic risks, and clinical statuses of the study subjects
Summary
Metabolic syndrome, which is characterized by visceral adiposity, is widely recognized as a risk factor for diverse metabolic disorders including type 2 diabetes, hypertension, and dyslipidemia, and causes atherosclerotic diseases. Using medicines with beneficial pleiotropic effects on adipose tissue or vasculature, such as suppressing inflammation or decreasing oxidative stress, would be more essential for the treatment of each metabolic disorder and protection of atherosclerosis. We aimed to identify difference in effects on biochemical markers of inflammation, oxidative stress, and atherosclerosis between two DPP-4 inhibitors in patients with type 2 diabetes. Results: Among markers, serum levels of high molecular weight (HMW) adiponectin significantly increased from 6.9 ± 3.6 μg/ml to 8.2 ± 4.0 μg/ml (P = 0.0045). No clinical data changed after 3 months, significant improvements in HbA1c and BMI were observed after 12 months Their rates of changes tended to inversely correlate with the increased percentages of serum HMW adiponectin levels during initial 3 months, but they did
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
