Troglitazone enhances glucose uptake and inhibits mitogen-activated protein kinase in human aortic smooth muscle cells
Autor: | Ritsu Tamura, Tohru Funahashi, Yuji Matsuzawa, Etsuko Shinohara, Shinji Kihara, Noriyuki Ouchi, Shizuya Yamashita |
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Rok vydání: | 1998 |
Předmět: |
DNA Replication
medicine.medical_specialty Arteriosclerosis medicine.drug_class Glucose uptake medicine.medical_treatment Biology Muscle Smooth Vascular Troglitazone Insulin resistance Internal medicine medicine Humans Hypoglycemic Agents Insulin Chromans Kinase activity Thiazolidinedione Aorta Cells Cultured Glucose transporter medicine.disease Thiazoles Insulin receptor Glucose Endocrinology Calcium-Calmodulin-Dependent Protein Kinases cardiovascular system biology.protein Thiazolidinediones Insulin Resistance Cardiology and Cardiovascular Medicine Cell Division medicine.drug |
Zdroj: | Atherosclerosis. 136:163-168 |
ISSN: | 0021-9150 |
Popis: | The thiazolidinedione analogue troglitazone is an antidiabetic agent that improves insulin resistance in rodents and humans. Although coronary artery disease is common in patients with the insulin resistance syndrome, the effects of troglitazone on smooth muscle cells (SMC) have not been fully elucidated. We therefore examined the effects of troglitazone on cell growth and glucose uptake in human aortic SMC. Mitogen-activated protein (MAP) kinase activity and glucose transporter (Glut) 1 mRNA levels were also studied. In the absence of troglitazone, insulin (10 −7 M) caused a 2-fold increase of DNA synthesis in SMC and troglitazone suppressed the increase of DNA synthesis in a dose-dependent manner. This growth suppression was accompanied by inhibition of MAP kinase activity. On the other hand, troglitazone significantly increased Glut 1 mRNA and enhanced glucose uptake in SMC. These results suggest that troglitazone affects the insulin signaling pathways in SMC and suppresses growth while promoting glucose uptake. Our findings support the application of troglitazone as an inhibitor of SMC proliferation in patients with insulin resistance. |
Databáze: | OpenAIRE |
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