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      Differential effects of rosiglitazone and insulin glargine on inflammatory markers, glycemic control, and lipids in type 2 diabetes.

      Diabetes Research and Clinical Practice
      Biological Markers, blood, Blood Glucose, metabolism, C-Reactive Protein, Cholesterol, Diabetes Mellitus, Type 2, drug therapy, Hemoglobin A, Glycosylated, drug effects, Humans, Hypoglycemic Agents, therapeutic use, Inflammation, Insulin, analogs & derivatives, Insulin, Long-Acting, Lipids, Plasminogen Activator Inhibitor 1, Thiazolidinediones, Triglycerides

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          Abstract

          Type 2 diabetes remains a difficult clinical challenge characterized by progressive insulin deficiency and frequent cardiovascular events requiring multiple therapeutic decisions. In this randomized clinical trial, we assessed the comparative effects of rosiglitazone (RSG) and insulin glargine (IG) on inflammatory biomarkers, glycemic control, and lipids. Forty subjects with type 2 diabetes and inadequate glycemic control on sulfonylurea and metformin therapy received 24 weeks of add-on therapy with either RSG 4mg daily or IG 10 units daily. Subjects on RSG with fasting glucose values >120mg/dl at 12 weeks were increased from 4 to 8mg. Subjects on IG increased insulin doses until fasting glucose was <120mg/dl. Markers of glycemic control and inflammation including HbA1c, hsCRP, PAI-1, plasma F2-isoprostanes, and lipids were measured at baseline, 12, 18, and 24 weeks. RSG and IG demonstrated similar efficacy in reducing HbA1c levels by 1.5 and 1.4%, respectively, with greater weight gain with RSG. Hypoglycemic events occurred with equal frequency. IG did not reduce hsCRP, but RSG reduced hsCRP levels 45% from baseline. Both IG and RSG reduced F2-isoprostanes similarly. IG did not affect PAI-1 levels, but did reduce total, LDL, and non-HDL cholesterol levels. Despite similar HbA1c reductions with RSG and IG, differential effects were found on inflammatory biomarkers and lipids that deserve consideration in the clinical decision process of selecting a therapeutic agent.

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