We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Insulin and its analogue glargine do not affect viability and proliferation of human coronary artery endothelial and smooth muscle cells.
- Authors
Staiger, K.; Staiger, H.; Schweitzer, M. A.; Metzinger, E.; Balletshofer, B.; Häring, H.-U.; Kellerer, M.
- Abstract
Aims/hypothesis: Present guidelines for the treatment of type 2 diabetes recommend HbA1c values of less than 7%. As beta cell function worsens during progress of the disease, insulin therapy is often necessary to achieve this ambitious goal. However, due to peripheral insulin resistance, many patients need rather high insulin dosages. In the light of the extremely high cardiovascular risk of diabetic patients, it is important to determine whether high concentrations of insulin or its frequently used analogues are harmful to the cardiovascular system. We therefore investigated the modulatory effects of regular human insulin and its analogue glargine on proliferation and apoptosis of human coronary artery endothelial cells (HCAECs) and human coronary artery smooth muscle cells (HCASMCs). Methods: Cells were treated with regular human insulin or insulin glargine. Proliferation was determined by [³H]thymidine incorporation and by flow cytometric analysis of Ki-67 expression. Apoptosis was assessed by flow cytometry (cell cycle analysis and annexin V staining) and determination of caspase-3 activity. Results: HCAECs and HCASMCs treated with regular human insulin or insulin glargine did not show significant increases in DNA synthesis or Ki-67 expression. Administration of regular human insulin or insulin glargine did not modulate the extent of apoptotic events. No influence of insulin on lipoapoptotic vascular cell death could be detected. Conclusions/interpretation: Taken together, neither regular human insulin nor insulin glargine influences growth and apoptosis of human coronary artery cells in vitro. Our data do not suggest that regular human insulin or insulin glargine promote atherosclerosis through mechanisms affecting the cellularity of human coronary arteries.
- Subjects
THERAPEUTICS; TYPE 2 diabetes; CORONARY arteries; INSULIN therapy; INSULIN resistance; THYMIDINE; APOPTOSIS; ATHEROSCLEROSIS
- Publication
Diabetologia, 2005, Vol 48, Issue 9, p1898
- ISSN
0012-186X
- Publication type
Article
- DOI
10.1007/s00125-005-1874-4