%0 Journal Article
%T Alogliptin ameliorates postprandial lipemia and postprandial endothelial dysfunction in non- diabetic subjects: a preliminary report
%A Yoko Noda
%A Toru Miyoshi
%A Hiroki Oe
%A Yuko Ohno
%A Kazufumi Nakamura
%A Norihisa Toh
%A Kunihisa Kohno
%A Hiroshi Morita
%A Kengo Kusano
%A Hiroshi Ito
%J Cardiovascular Diabetology
%D 2013
%I BioMed Central
%R 10.1186/1475-2840-12-8
%X A randomized cross-over trial design in 10 healthy volunteers (8 males and 2 females, 35 ¡À 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.Alogliptin treatment significantly suppressed the postprandial elevation in serum triglyceride (incremental area under the curve [AUC]; 279 ¡À 31 vs. 182 ¡À 32 mg h/dl, p = 0.01), apoB-48 (incremental AUC; 15.4 ¡À 1.7 vs. 11.7 ¡À 1.1 ¦Ìg h/ml, p = 0.04), and remnant lipoprotein cholesterol (RLP-C) (incremental AUC: 29.3 ¡À 3.2 vs. 17.6 ¡À 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 ¡À 0.5% to £¿2.6 ¡À 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).Alogliptin significantly improved postprandial endothelial dysfunction and postprandial lipemia, suggesting that alogliptin may be a promising anti-atherogenic agent.Large prospective studies have shown that non-fasting postprandial triglyceride (TG) concentrations predict cardiovascular risk better than fasting TG concentrations and that this relationship is independent of traditional coronary risk factors [1,2]. TG-rich lipoproteins, which consist of chylomicrons assembled by TG, dietary cholesterol, and apolipoprotein B-48 (apoB-48), are highly atherogenic and contribute to the development of coronary heart disease. Thus, the increased risk of cardiovascular events associated with non-fasting TG concentrations may reflect atherogenic properties of TG-rich lipoproteins generated during the postprandial period [3]. Studies have shown that postpr
%K Dipeptidyl peptidase IV inhibitor
%K Postprandial lipid
%K Triglyceride-rich lipoprotein
%K Endothelial dysfunction
%K Alogliptin
%U http://www.cardiab.com/content/12/1/8