Fibrate therapy in patients with metabolic syndrome and diabetes mellitus

被引：13

作者：

Dayspring T. ^{[1
]}

Pokrywka G. ^{[1
]}

机构：

[1] North Jersey Institute of Menopausal Lipidology, Wayne, NJ 07470

来源：

Current Atherosclerosis Reports | 2006年 / 8卷 / 5期

关键词：

Statin; Ezetimibe; Arterioscler Thromb Vasc Biol; Fibrate Therapy; Diabetes Atherosclerosis Intervention Study;

D O I：

10.1007/s11883-006-0032-x

中图分类号：

学科分类号：

摘要：

Patients with metabolic syndrome and type 2 diabetes mellitus are usually in moderately high-risk, high-risk, or very high-risk cardiovascular categories and present major therapeutic challenges. The dyslipidemia in such patients is typically a disorder of the triglyceride/high-density lipoprotein axis (TG/HDL axis) characterized by an excess of triglyceride-rich lipoproteins and a reduction of HDL. Very often, lifestyle therapy and statin monotherapy fail to achieve guideline goals, necessitating combination therapies. Fibric acids (or fibrates), are agonists of peroxisome proliferator-activated receptor α, which have amassed significant lipid-surrogate and clinical outcome trial data, especially in insulin-resistant patients, typical of those with metabolic syndrome or type 2 diabetes mellitus. Current guidelines advocate fibrate use as an add-on to statin therapy when TG/HDL abnormalities exist in such patients. In this paper, we review pertinent and recent trial data, mechanisms of action, and the safety of fibrate therapy. Copyright © 2006 by Current Science Inc.

引用

页码：356 / 364

页数：8

共 71 条

[31]

Koh K.K., Quon M.J., Han S.H., Et al., Additive beneficial effects of fenofibrate combined with atorvastatin in the treatment of combined hyperlipidemia, J Am Coll Cardiol, 45, pp. 1649-1653, (2005)

[32]

Farnier M., Freeman M.W., Macdonell G., Et al., Efficacy and safety of the coadministration of ezetimibe with fenofibrate in patients with mixed hyperlipidaemia, Eur Heart J, 26, pp. 897-905, (2005)

[33]

Spencer G.A., Wirebaugh S., Whitney E.J., Effect of a combination of gemfibrozil and niacin on lipid levels, J Clin Pharmacol, 36, pp. 696-700, (1996)

[34]

Whitney E.J., Krasuski R.A., Personius B.E., Et al., A randomized trial of a strategy for increasing high-density lipoprotein cholesterol levels: Effects on progression of coronary heart disease and clinical events, Ann Intern Med, 142, pp. 95-104, (2005)

[35]

Berger J., Moller D.E., The mechanisms of action of PPARs, Annu Rev Med, 53, pp. 409-435, (2002)

[36]

Lefebvre P., Chinetti G., Fruchart J.C., Staels B., Sorting out the roles of PPAR-a in energy metabolism and vascular homeostasis, J Clin Invest, 116, pp. 571-580, (2006)

[37]

Ramaswamy G., Karim M.A., Gopal Murti K., Jackowski S., PPARa controls the intracellular coenzyme A concentration via regulation of PANK1a gene expression, J Lipid Res, 45, pp. 17-31, (2004)

[38]

Li Y., Nara T.Y., Nakamura M.T., Peroxisome proliferator-activated receptor alpha is required for feedback regulation of highly unsaturated fatty acid synthesis, J Lipid Res, 46, pp. 2432-2440, (2005)

[39]

Zhu D., Ganji S.H., Kamanna V.S., Kashyap M.L., Effect of gemfibrozil on apolipoprotein B secretion and diacylglycerol acyltransferase activity in human hepatoblastoma (HepG2) cells, Atherosclerosis, 164, pp. 221-228, (2002)

[40]

Guerin M., Bruckert E., Dolphin P.J., Et al., Fenofibrate reduces plasma cholesteryl ester transfer from HDL to VLDL and normalizes the atherogenic dense LDL profile in combined hyperlipidemia, Arterioscler Thromb Vasc Biol, 16, pp. 763-772, (1996)

← 1 2 3 4 5 6 7 8 →