title: Alogliptin ameliorates postprandial lipemia and postprandial endothelial dysfunction in non-diabetic subjects: a preliminary report.
abstract: BACKGROUND
  Postprandial hyperlipidemia impairs endothelial function and participates in the development of atherosclerosis. We investigated the postprandial effects of a dipeptidyl peptidase IV inhibitor, alogliptin, on endothelial dysfunction and the lipid profile.
  
  
  METHODS
  A randomized cross-over trial design in 10 healthy volunteers (8 males and 2 females, 35 ± 10 years) was performed. The postprandial effects before and after a 1-week treatment of 25 mg/day alogliptin on endothelial function were assessed with brachial artery flow-mediated dilation (FMD) and changing levels of lipids, apolipoprotein B48 (apoB-48), glucose, glucagon, insulin, and glucagon-like peptide-1 (GLP-1) during fasting and at 2, 4, 6, and 8 h after a standard meal loading test.
  
  
  RESULTS
  Alogliptin treatment significantly suppressed the postprandial elevation in serum triglyceride (incremental area under the curve [AUC]; 279 ± 31 vs. 182 ± 32 mg h/dl, p = 0.01), apoB-48 (incremental AUC; 15.4 ± 1.7 vs. 11.7 ± 1.1 μg h/ml, p = 0.04), and remnant lipoprotein cholesterol (RLP-C) (incremental AUC: 29.3 ± 3.2 vs. 17.6 ± 3.3 mg h/dl, p = 0.01). GLP-1 secretion was significantly increased after alogliptin treatment. Postprandial endothelial dysfunction (maximum decrease in%FMD, from -4.2 ± 0.5% to -2.6 ± 0.4%, p = 0.03) was significantly associated with the maximum change in apoB-48 (r = -0.46, p = 0.03) and RLP-C (r = -0.45, p = 0.04).
  
  
  CONCLUSIONS
  Alogliptin significantly improved postprandial endothelial dysfunction and postprandial lipemia, suggesting that alogliptin may be a promising anti-atherogenic agent.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Noda
authors.forename: Toru
authors.initials: T
authors.lastname: Miyoshi
authors.forename: Hiroki
authors.initials: H
authors.lastname: Oe
authors.forename: Yuko
authors.initials: Y
authors.lastname: Ohno
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Norihisa
authors.initials: N
authors.lastname: Toh
authors.forename: Kunihisa
authors.initials: K
authors.lastname: Kohno
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Kengo
authors.initials: K
authors.lastname: Kusano
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ito
mesh_terms: D000328:Adult; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy*; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D010880:Piperidines / Q000494:pharmacology / Q000627:therapeutic use*; D019518:Postprandial Period / Q000187:drug effects* / Q000502:physiology; D014498:Uracil / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D007004:Hypoglycemic Agents; D010880:Piperidines; D014498:Uracil; C520853:alogliptin