Q. Qiao, S. Larsen, K. Borch-Johnsen et al., “Glucose tolerance and cardiovascular mortality. Comparison of fasting and 2-hour diagnostic criteria,” Archives of Internal Medicine, vol. 161, no. 3, pp. 397–405, 2001.
has been cited by the following article:
- TITLE: Short-Term Effect of Pitavastatin Treatment on Glucose and Lipid Metabolism and Oxidative Stress in Fasting and Postprandial State Using a Test Meal in Japanese Men
- AUTHORS: Hirokazu Kakuda,Junji Kobayashi,Mio Nakato,Noboru Takekoshi
JOURNAL NAME: Cholesterol
Sep 16, 2014
- ABSTRACT: Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2？mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2？mg once daily) with a test meal consisting of total calories: 460？kcal, carbohydrates: 56.5？g (226？kcal), protein: 18？g (72？kcal), lipids: 18？g (162？kcal), and NaCl: 1.6？g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance ( ) and uric acid clearance ( ) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides ( ) and remnant-like particle cholesterol ( ), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia. 1. Introduction It has been generally recognized that postprandial hyperglycemia and hyperlipidemia are highly related to the development of atherosclerosis [1–5]. Hyperglycemia is known to damage vascular endothelial cells, increase oxidative stress, promote the expression of adhesion molecules, and inhibit Nitric Oxide (NO) production . Remnant lipoprotein, an important component of postprandial hyperlipidemia, promotes foam cell formation of macrophages and proliferation of smooth muscle cells . A very recent study on a large number of subjects demonstrated that remnant cholesterol was a causal risk factor for ischemic heart disease . Lipid-lowering drugs, such as statins, fibrates, and ezetimibe are considered to be useful for the treatment of postprandial hyperlipidemia [9–15]. Pitavastatin, a member of the medication class of statins, has been available in the market in Japan since 2003. It has been well recognized that this statin is markedly effective in reducing low-density lipoprotein