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Original Articles

Alogliptin: a new dipeptidyl peptidase-4 inhibitor with potential anti-atherogenic properties

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Pages 88-96 | Received 14 Jan 2014, Accepted 05 Aug 2014, Published online: 10 Sep 2014
 

Abstract

Objectives: The aim of this study is to evaluate the effects of alogliptin on metabolic profiles in relation to those of glycemic control. Patients and methods: Treatment naïve subjects with type 2 diabetes received 12.5–25 mg/d alogliptin monotherapy (n = 59). A novel parameter called A1c index was used to assess the glycemic efficacy. The subjects were divided into three groups according to this index; super-responders, average responders and poor-responders. At 3 months, levels of the metabolic parameters were compared with those at baseline between super-responders (n = 20) and poor-responders (n = 21). Results: At baseline, total cholesterol, non-high density lipoprotein cholesterol and atherogenic index were significantly higher in super-responders than poor-responders. At 3 months, significant increases of beta-cell function (HOMA-B) and decreases of insulin resistance (HOMA-R) or these atherogenic lipids were observed in super-responders, while significant increases of HOMA-R were observed in poor-responders. Significant correlations were observed between A1c index and the changes of these atherogenic lipids. In super-responders, significant correlations were observed between the changes (Δ) of glycemic parameters (A1c index or fasting blood sugar) and ΔHOMA-R and/or ΔHOMA-B, while in poor-responders, significant correlations were observed between ΔHOMA-R and ΔHOMA-B. Lean subjects gained weight and the changes of body mass index had significant negative correlations with A1c index. Conclusions: These results indicate that (1) glucose lowering efficacy of alogliptin is closely linked to atherogenic lipids. (2) alogliptin can down-regulate atherogenic lipids. (3) glycemic efficacy of alogliptin appears to be determined by the balance of its capacity in modulating insulin resistance and beta-cell function.

Acknowledgements

The authors thank Drs. Jan Wajs, Hiroshi Kawashima, Takashi Suzuki, Asuka Wada, Yu Ikeo, and Sachiko Yokoyama for supports and discussions.

Declaration of interest

The authors declare that there are no conflicts of interests regarding this work.

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