PPAR ligands: Potential therapies for metabolic syndrome

被引：48

作者：

Akiyama T.E. ^{[1
]}

Meinke P.T. ^{[1
]}

Berger J.P. ^{[1
]}

机构：

[1] Merck Research Laboratories, Rahway, NJ 07065

来源：

Current Diabetes Reports | 2005年 / 5卷 / 1期

关键词：

Metabolic Syndrome; Rosiglitazone; Pioglitazone; Telmisartan; Troglitazone;

D O I：

10.1007/s11892-005-0067-3

中图分类号：

学科分类号：

摘要：

Metabolic syndrome (MS), a condition characterized by multiple related clinical disorders including insulin resistance, central obesity, hyperlipidemia, hypertension, and heart disease, is an increasingly prevalent disease in industrialized societies. The intense research interest in the peroxisome proliferator-activated receptors (PPARs), by both the pharmaceutical industry and academia, stems largely from the well-documented therapeutic actions of their synthetic agonists in alleviating several of the maladies associated with MS. This report focuses on the current understanding of the mechanisms of action of PPAR agents and their clinical use in the context of MS. Copyright © 2005 by Current Science Inc.

引用

页码：45 / 52

页数：7

共 73 条

[21]

Lehmann J.M., Moore L.B., Smith-Oliver T.A., Et al., An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma), J. Biol. Chem., 270, pp. 12953-12956, (1995)

[22]

Inzucchi S.E., Maggs D.G., Spollett G.R., Et al., Efficacy and metabolic effects of metformin and troglitazone in type II diabetes mellitus, N. Engl. J. Med., 338, pp. 867-872, (1998)

[23]

Chao L., Marcus-Samuels B., Mason M.M., Et al., Adipose tissue is required for the antidiabetic, but not for the hypolipidemic, effect of thiazolidinediones, J. Clin. Invest., 106, pp. 1221-1228, (2000)

[24]

Rangwala S.M., Lazar M.A., Peroxisome proliferator-activated receptor gamma in diabetes and metabolism, Trends Pharmacol. Sci., 25, pp. 331-336, (2004)

[25]

Matsusue K., Haluzik M., Lambert G., Et al., Liver-specific disruption of PPARgamma in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypes, J. Clin. Invest., 111, pp. 737-747, (2003)

[26]

Norris A.W., Chen L., Fisher S.J., Et al., Muscle-specific PPAR-gamma-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones, J. Clin. Invest., 112, pp. 608-618, (2003)

[27]

Okuno A., Tamemoto H., Tobe K., Et al., Troglitazone increases the number of small adipocytes without the change of white adipose tissue mass in obese Zucker rats, J. Clin. Invest., 101, pp. 1354-1361, (1998)

[28]

Mayerson A.B., Hundal R.S., Dufour S., Et al., The effects of rosiglitazone on insulin sensitivity, lipolysis, and hepatic and skeletal muscle triglyceride content in patients with type 2 diabetes, Diabetes, 51, pp. 797-802, (2002)

[29]

Kawai T., Takei I., Oguma Y., Et al., Effects of troglitazone on fat distribution in the treatment of male type 2 diabetes, Metabolism, 48, pp. 1102-1107, (1999)

[30]

Laplante M., Sell H., MacNaul K.L., Et al., PPAR-gamma activation mediates adipose depot-specific effects on gene expression and lipoprotein lipase activity: Mechanisms for modulation of postprandial lipemia and differential adipose accretion, Diabetes, 52, pp. 291-299, (2003)

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