title: Alogliptin: a new dipeptidyl peptidase-4 inhibitor with potential anti-atherogenic properties.
abstract: OBJECTIVE
  The aim of this study is to evaluate the effects of alogliptin on metabolic profiles in relation to those of glycemic control.
  
  
  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.
authors.affiliation: Biomedical Center , Tokyo , Japan and.
authors.forename: Eiji
authors.initials: E
authors.lastname: Kutoh
authors.forename: Noriko
authors.initials: N
authors.lastname: Kaneoka
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Hirate
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000517:prevention & control*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D003925:Diabetic Angiopathies / Q000517:prevention & control*; D054873:Dipeptidyl-Peptidase IV Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000502:physiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010880:Piperidines / Q000009:adverse effects / Q000627:therapeutic use*; D014498:Uracil / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D001786:Blood Glucose; D054873:Dipeptidyl-Peptidase IV Inhibitors; D006442:Glycated Hemoglobin; D008055:Lipids; D010880:Piperidines; D014498:Uracil; C520853:alogliptin
keywords: Alogliptin; DPP-4 inhibitors; atherogenic lipids