A Comparison of Lipid and Glycemic Effects of Pioglitazone and Rosiglitazone in Patients With Type 2 Diabetes and Dyslipidemia
- Ronald B. Goldberg, MD1,
- David M. Kendall, MD2,
- Mark A. Deeg, MD, PHD3,
- John B. Buse, MD, PHD4,
- Anthony J. Zagar, MS5,
- Jane A. Pinaire, PHD5,
- Meng H. Tan, MD5,
- Mehmood A. Khan, MD6,
- Alfonso T. Perez, MD7,
- Scott J. Jacober, DO5 and
- for the GLAI Study Investigators
- 1Division of Endocrinology, Metabolism, and Diabetes, University of Miami School of Medicine, Miami, Florida
- 2International Diabetes Center, Park Nicollet Institute, Minneapolis, Minnesota
- 3Division of Endocrinology and Metabolism, Department of Veterans Affairs and the Indiana University School of Medicine, Indianapolis, Indiana
- 4Divisions of Endocrinology and of General Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina
- 5Lilly Research Laboratories, Eli Lilly, Indianapolis, Indiana
- 6Takeda Pharmaceuticals North America, Lincolnshire, Illinois
- 7Takeda Global Research and Development Center, Lincolnshire, Illinois
- Address correspondence and reprint requests to Scott J. Jacober, DO, Lilly Research Laboratories, A Division of Eli Lilly, Lilly Corporate Center, DC 5116, Indianapolis, IN 46285. E-mail: sjacober{at}lilly.com
Abstract
OBJECTIVE—Published reports suggest that pioglitazone and rosiglitazone have different effects on lipids in patients with type 2 diabetes. However, these previous studies were either retrospective chart reviews or clinical trials not rigorously controlled for concomitant glucose- and lipid-lowering therapies. This study examines the lipid and glycemic effects of pioglitazone and rosiglitazone.
RESEARCH DESIGN AND METHODS—We enrolled subjects with a diagnosis of type 2 diabetes (treated with diet alone or oral monotherapy) and dyslipidemia (not treated with any lipid-lowering agents). After a 4-week placebo washout period, subjects randomly assigned to the pioglitazone arm (n = 400) were treated with 30 mg once daily for 12 weeks followed by 45 mg once daily for an additional 12 weeks, whereas subjects randomly assigned to rosiglitazone (n = 402) were treated with 4 mg once daily followed by 4 mg twice daily for the same intervals.
RESULTS—Triglyceride levels were reduced by 51.9 ± 7.8 mg/dl with pioglitazone, but were increased by 13.1 ± 7.8 mg/dl with rosiglitazone (P < 0.001 between treatments). Additionally, the increase in HDL cholesterol was greater (5.2 ± 0.5 vs. 2.4 ± 0.5 mg/dl; P < 0.001) and the increase in LDL cholesterol was less (12.3 ± 1.6 vs. 21.3 ± 1.6 mg/dl; P < 0.001) for pioglitazone compared with rosiglitazone, respectively. LDL particle concentration was reduced with pioglitazone and increased with rosiglitazone (P < 0.001). LDL particle size increased more with pioglitazone (P = 0.005).
CONCLUSIONS—Pioglitazone and rosiglitazone have significantly different effects on plasma lipids independent of glycemic control or concomitant lipid-lowering or other antihyperglycemic therapy. Pioglitazone compared with rosiglitazone is associated with significant improvements in triglycerides, HDL cholesterol, LDL particle concentration, and LDL particle size.
- CHD, coronary heart disease
- CVD, cardiovascular disease
- LOCF, last observation carried forward
- PAI-1, plasminogen activator inhibitor-1
Footnotes
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A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
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- Accepted March 31, 2005.
- Received February 10, 2005.
- DIABETES CARE














