The Gene Expression Patterns in the Peripheral White Blood Cells of Type 2 Diabetic Patients
Recruitment status was: Recruiting
Diabetes Mellitus, Type 2
|Study Design:||Observational Model: Case Control
Observational Model: Natural History
Time Perspective: Longitudinal
Time Perspective: Prospective
|Official Title:||The Gene Expression Patterns in the Peripheral White Blood Cells of Type 2 Diabetic Patients, Special Relevance to Atherosclerosis|
|Study Start Date:||November 2003|
Cardiovascular events are the leading cause of death in developed countries worldwide, including Taiwan. Type 2 diabetes mellitus (T2DM), previously considered merely as one of the risk factors, has been recently unanimously accepted to be coronary artery disease-equivalent. How T2DM may lead to accelerated atherosclerosis remains obscure.
Hyperglycemia with or without hyperinsulinemia may lead to higher oxidative stress and generalized inflammation. The oxidative stress and inflammation may play a significant role in the pathogenesis in diabetic complications, including micro- and macro-vascular complications. Macrophages together with T-lymphocytes are the earliest cell-types found in fatty-streaks, the earliest atherosclerotic lesions. Macrophages are also well known cellular mediators of oxidative stress and inflammation. Therefore, it is plausible to hypothesize that macrophages play a crucial role in the pathogenesis of atherosclerosis in patients with T2DM. In addition, the other cell types of the peripheral white blood cells (WBC), such as neutrophils, have been shown to be intimately related to acute coronary syndrome. Therefore, the study on the biology of peripheral WBCs may tell us something about the pathophysiology of diabetic macro-vascular complications.
- Normal control: fasting plasma glucose (FPG) less than 126 mg/dl.
T2DM: FPG ＞＝126 mg/dl.
- Group 1 (good glycemic control): hemoglobin A1c (HbA1c) ＜＝ 7% in the past 6 months
- Group 2 (poor glycemic control): HbA1c ＞＝ 8% in the past 6 months
- Blood sample will be collected at baseline and after aggressive control.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00155922
|National Taiwan University Hospital|
|Taipei, Taiwan, 10012|
|Principal Investigator:||Wei-Shiung Yang, MD, PhD||National Taiwan University Hospital|