Pioglitazone Study of Triglyceride Changes in Subjects With Type 2 Diabetes After Conversion From Rosiglitazone. (COMPLEMENT)
|Study Design:||Allocation: Non-Randomized
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||A Single-Arm, Open-Label, Multicenter Study Evaluating the Triglyceride Changes in Subjects With Type 2 Diabetes Mellitus and Dyslipidemia Following Treatment Conversion From Rosiglitazone to Pioglitazone HCl in Combination With Stable Statin Therapy|
- Change from Baseline in Triglyceride Levels [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in Total Cholesterol [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in direct Low Density Lipoprotein cholesterol [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in High Density Lipoprotein cholesterol [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in apolipoprotein B (apoB) [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in apolipoprotein A1 (apoA1) [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in Free Fatty Acids [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in Lipid Fractionation [ Time Frame: Weeks 8 and 17 or Final Visit ]
- Change from Baseline in C-reactive Protein [ Time Frame: Weeks 8 and 17 or Final Visit ]
|Study Start Date:||November 2003|
|Study Completion Date:||August 2004|
|Primary Completion Date:||August 2004 (Final data collection date for primary outcome measure)|
Experimental: Pioglitazone QD
(and stable statin therapy)
Pioglitazone 30 mg to 45 mg, tablets, orally, once daily in combination with stable statin therapy for up to 17 weeks.
Diabetes mellitus is a chronic disease with multiple metabolic defects that result in hyperglycemia arising from inadequate insulin activity. Type 2 diabetes has a genetic predisposition, but lifestyle, physical habits and age play important roles in determining its time of onset and severity. Type 2 diabetes is usually the result of a progression from reduced sensitivity of hepatic (liver) and peripheral-tissue cells to circulating insulin (ie, insulin resistance) to a progressive inability of the body to produce adequate insulin to overcome insulin resistance (ie, insulin deficiency due to beta-cell insufficiency) resulting in impaired glucose tolerance and ultimately overt diabetes. In the United States, an estimated 15.7 million people have diabetes, with type 2 diabetes occurring in approximately 90 to 95% of cases.
Therapeutic agents have been developed to address each of the major functional metabolic defects associated with type 2 diabetes. Recently introduced drugs for diabetes therapy are the thiazolidinedione class. Thiazolidinediones increase glucose utilization, decrease gluconeogenesis and increase glucose disposal through an incompletely understood mechanism but one associated with binding of the drug to receptors known as peroxisomal proliferator-activated receptors.
Thiazolidinediones are peroxisomal proliferator-activated receptor agonists reducing insulin resistance in muscle cells, adipose (fat) tissue, and hepatic cells (inhibiting hepatic gluconeogenesis) with no direct impact on insulin secretion. Thus peroxisomal proliferator-activated receptor agonists improve glycemic control and result in reduced levels of circulating insulin. Peroxisomal proliferator-activated receptors are found in various tissues important for insulin action, with the greatest concentration of these receptors is in adipose tissue.
Pioglitazone is a peroxisomal proliferator-activated receptor agonist developed by Takeda Chemical Industries, Ltd. (Osaka, Japan).
Participation in this study is anticipated to be approximately 20 weeks.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00672919
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|Study Director:||VP Clinical Science Strategy||Takeda|