Pitavastatin prevents postprandial endothelial dysfunction via reduction of the serum triglyceride level in obese male subjects

• Published in: Heart and vessels Vol. 26; no. 4; pp. 428 - 434
• Main Authors: Nagashima, Hirotaka, Endo, Masahiro
• Format: Journal Article
• Language: English
• Published: Japan Springer Japan 01.07.2011; Springer Nature B.V
• Subjects: Adult; Aged; Biomarkers - blood; Biomedical Engineering and Bioengineering; Blood; Blood diseases; Cardiac Surgery; Cardiology; Cellular biology; Clinical outcomes; Dietary Fats - administration & dosage; Down-Regulation; Drug therapy; Endothelium, Vascular - diagnostic imaging; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiopathology; Heart; Heart diseases; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Hypertriglyceridemia - blood; Hypertriglyceridemia - drug therapy; Hypertriglyceridemia - etiology; Hypertriglyceridemia - physiopathology; Japan; Lipids; Male; Medicine; Medicine & Public Health; Middle Aged; Obesity; Obesity - blood; Obesity - complications; Obesity - drug therapy; Obesity - physiopathology; Original Article; Postprandial Period; Quinolines - therapeutic use; Regression Analysis; Risk factors; Statins; Therapy; Time Factors; Treatment Outcome; Triglycerides; Triglycerides - blood; Ultrasonography; Vascular Surgery; Vasodilation - drug effects; Work load; Pitavastatin; Triglycerides; Endothelial function; Postprandial response
• ISSN: 0910-8327; 1615-2573; 1615-2573
• DOI: 10.1007/s00380-010-0071-7

Obesity is a well-established risk factor for the development and progression of coronary heart disease. Moreover, endothelial dysfunction is an early event in atherosclerosis and is known to be associated with postprandial hypertriglyceridemia. The purpose of this study was to determine whether a statin might have an effect on postprandial hypertriglyceridemia, and thereby on endothelial function in obese subjects. Twenty-four obese male subjects were recruited for this study. They were randomly assigned to receive pitavastatin (2 mg/day) or placebo for 2 weeks. The oral fat loading test using OFTT cream was performed pre- and post-treatment, in which the lipid profile and flow-mediated dilation (FMD) were assessed before and 4 h after an oral fat load. In the oral fat loading test conducted pretreatment, the oral fat load induced a marked increase of the serum triglyceride (TG) level and decrease in FMD in the pitavastatin and placebo group. In the test conducted post-treatment, the increase in postprandial TG was attenuated (+183 vs. +81 mg/dL, P  < 0.001) and decrease in postprandial FMD was completely abolished (−1.1 vs. +0.1%, P  < 0.01) by pitavastatin treatment. Moreover, there was a good correlation between the change in postprandial TG and the change in postprandial FMD after the 2 weeks of treatment ( r  = −0.737, P  < 0.001). Pitavastatin might prevent endothelial dysfunction caused by postprandial hypertriglyceridemia within 2 weeks of therapy in obese subjects.