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Ciglitazone

The medication class of thiazolidinedione was introduced in the late 1990s as an adjunctive therapy for diabetes mellitus (type II) and related diseases. more...

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Mode of action

Thiazolidinediones act by binding to PPARs (peroxisome proliferator-activated receptors), a group of receptor molecules inside the cell nucleus, specifically PPARγ (gamma). The normal ligands for these receptors are free fatty acids (FFAs) and eicosanoids. When activated, the receptor migrates to the DNA, activating transcription of a number of specific genes.

Genes upregulated by PPARγ can be found in the main article on peroxisome proliferator-activated receptors.

By activating PPARγ:

  • insulin resistance is decreased
  • adipocyte differentiation is modified
  • VEGF-induced angiogenesis is inhibited (abstract).
  • Leptin levels decrease (leading to an increased appetite)
  • Levels of certain interleukins (e.g. IL-6) fall
  • Adiponectin levels rise

Members of the class

These include:

  • rosiglitazone
  • pioglitazone

Troglitazone was withdrawn from the market due to an increased incidence of drug-induced hepatitis in patients who were using the drug. It is now common practice that liver enzymes are monitored during the first year of treatment with the "newer" thiazolidinediones.

Experimental agents include MCC-555, a powerful antidiabetic agent and the early non-marketed thiazolidinedione ciglitazone.

Uses

The only registered use of the thiazolidinediones is in diabetes mellitus type 2.

It is being investigated experimentally in polycystic ovary syndrome (PCOS) and non-alcoholic steatohepatitis (NASH).

Several forms of lipodystrophy cause insulin resistance, which has responded favorably to thiazolidinediones.

Side-effects and contraindications

The withdrawal of troglitazone has led to concerns of other thiazolidinediones increasing the risk of hepatitis. Guidelines now mention that for the first year of thiazolidinedione therapy, a two- or three-monthly check of liver enzymes is conducted to ascertain that no liver damage is occurring.

The main side-effect of all thiazolidinediones is fluid retention, leading to edema and potentially aggravating heart failure. Therefore, thiazolidinediones cannot be prescribed in patients with decreased ventricular function (NYHA grade III and IV heart failure).

Read more at Wikipedia.org


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Ligands of peroxisome proliferator-activated receptor [gamma] inhibit lung cancer cell growth and induce apoptosis by stimulation of P21 expression
From CHEST, 5/1/04 by Shouwei Han

Abbreviations: 15d PGJ2 = 15 deoxy 12,14 prostaglandin J2; PPAR = peroxisome proliferator-activated receptor

Lung cancer is one of the most common malignant tumors in the world, and is the leading cause of cancer death in men and women in the United States. Despite recent advances in understanding the molecular biology of lung cancer and the introduction of multiple new chemotherapeutic agents for the treatment of non-small cell lung cancer, the dismal <15% 5-year survival rate has not changed substantially. New approaches toward the treatment and prevention of this disease are therefore clearly indicated. In many, studies, peroxisome proliferator-activated receptor (PPAR)-[gamma] has been implicated in the regulation of cell growth and differentiation. In our studies, we have shown that the PPAR-[gamma] ligands 15d-PGJ2, ciglitazone, and troglizaonc inhibited the growth of several human lung cancer cell Tines and induced apoptosis. Wy14643, one PPAR-[alpha] agonist, had no effects on those processes. The cell cycle control cyclin-dependent kinase inhibitor [P21.sup.waf1/Cip1] plays a role in cancer cell cycle arrest and apoptosis. In order to determine if effects on P:21 explain the human lung cancer growth inhibition observed with PPAR-[gamma] ligands, we examined the effects of these agents on P21 expression. We showed that treatment of lung cancer cells with PPAR-[gamma] ligands 15d-PGJ2, ciglitazone, and troglizaone induced P21 messenger RNA and protein levels, and reduced cyclin D1 messenger RNA levels as compared to the control. These effects were PPAR-[gamma] specific because WY14643 did not affect P21 expression. The PPAR-[gamma] antagonist GW9662 inhibited the effect of ciglitazone and troglitazone, but not that of 15d-PGJ2 on P21 gene expression. P21 antisense oligos inhibited both basal and PPAR-[gamma] ligands induced p21 messenger RNA and protein levels. Transient transfection assays indicated that PPAR-[gamma] ligands increased P21 promoter activity in human lung cancer cells. Gel mobility shift assay showed that PPAR-[gamma] ligands increased surfactant protein-1 binding activity in the P21 promoter region. Taken together, our results indicate that PPAR-[gamma] ligands inhibit human lung cancer cell growth and induce apoptosis by inducing the cyclin-dependent kinase inhibitor P21, and reducing cyclin D1 genes expression in PPAR-[gamma]--dependent and independent pathways.

* From the Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine (Drs. Han and Roman), and Department of Gynecology, and Obstetrics (Dr. Sidell), Emory University School of Medicine, Atlanta, GA: and Department of Pathology (Dr. Fisher), Herbert Irving Comprehensive Cancer Center, Columbia University College of Physicians and Surgeons, New York. NY.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: permissions@ehestnet.org).

Correspondence to: Shouwei Hart, MD, PhD, Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University School of Medicine, 615 Michael St., Suite 205M, Atlanta, GA 30322; e-mail: shan2@emncy.edu

COPYRIGHT 2004 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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