Diabetes Care
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Diabetes Care 29:1545-1553, 2006
DOI: 10.2337/dc05-2462
© 2006 by the American Diabetes Association
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Pathophysiology/Complications
Original Article

Effect of Peroxisome Proliferator–Activated Receptor {gamma} Agonist Treatment on Subclinical Atherosclerosis in Patients With Insulin-Requiring Type 2 Diabetes

Howard N. Hodis, MD1,2,3, Wendy J. Mack, PHD2,3, Ling Zheng, PHD2,4, Yanjie Li, MD3, Mina Torres, MS2,3, Diego Sevilla, PA1, Yolanda Stewart, BS1,4, Barbara Hollen, MPH1, Karla Garcia, BA1,4, Petar Alaupovic, PHD5 and Thomas A. Buchanan, MD1,4

1 Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California
2 Department of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles, California
3 Atherosclerosis Research Unit, University of Southern California Keck School of Medicine, Los Angeles, California
4 General Clinical Research Center, University of Southern California Keck School of Medicine, Los Angeles, California
5 Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma

Address correspondence and reprint requests to Howard N. Hodis, MD, Atherosclerosis Research Unit, University of Southern California Keck School of Medicine, 2250 Alcazar St., CSC 132, Los Angeles, CA 90033. E-mail: athero{at}usc.edu

OBJECTIVE—To determine the effect of thiazolidinedione treatment on subclinical atherosclerosis progression in insulin-requiring patients with clinical characteristics suggesting type 2 diabetes.

RESEARCH DESIGN AND METHODS—Eligible participants (n = 299) were randomized within strata of baseline common carotid artery (CCA) intima-media thickness (IMT) (<0.8 mm, ≥0.8 mm) to 400 mg troglitazone daily or placebo for 2 years. A general linear mixed-effects model was used to compare the rate of change in CCA-IMT between treatment groups.

RESULTS—Overall, average rates of CCA-IMT change were not significantly different between troglitazone- and placebo-treated subjects (0.0030 ± 0.021 vs. 0.0066 ± 0.021 mm/year; P = 0.17). In the stratum of subjects with CCA-IMT ≥0.8 mm, troglitazone significantly reduced the progression of CCA-IMT relative to placebo (0.0013 ± 0.022 vs. 0.0084 ± 0.023 mm/year; P = 0.03). Fasting glucose, insulin, and HbA1c were significantly lower in troglitazone- versus placebo-treated subjects (P < 0.01). Whereas blood pressure significantly differed between treatment groups in the ≥0.8-mm stratum, there was no difference between treatment groups in the <0.8-mm stratum.

CONCLUSIONS—Insulin sensitization and reduction in blood pressure may be contributory mechanisms by which troglitazone reduced subclinical atherosclerosis progression in this cohort of well-controlled insulin-dependent patients with clinical characteristics suggesting type 2 diabetes.

Abbreviations: ALT, alanine aminotransferase • CCA, common carotid artery • IMT, intima-media thickness • PPAR, peroxisome proliferator–activated receptor • TZD, thiazolidinedione


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Copyright © 2006 by the American Diabetes Association.