期刊
PROSTAGLANDINS & OTHER LIPID MEDIATORS
卷 87, 期 1-4, 页码 34-41出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2008.06.001
关键词
Prostaglandin; Diabetes; Insulin resistance; Glucose transport; Muscle; Adipose
资金
- American Diabetes Association [1-02-CD-11]
- Winthrop U. Hospital Medical Education Fund
Previously, we demonstrated that lipocalin-type prostaglandin D-2 synthase (L-PGDS) knockout mice become glucose intolerant and display signs of diabetic nephropathy and accelerated atherosclerosis. In the current study we sought to explain the link between L-PGDS and glucose tolerance. Using the insulin-sensitive rat skeletal muscle cell line, L6, we showed that L-PGDS could stimulate glucose transport approximately 2-fold as well as enhance insulin-stimulated glucose transport, as measured by 2-deoxy-[H-3]-glucose uptake. The increased glucose transport was not attributed to increased GLUT4 production but rather the stimulation of GLUT4 translocation to the plasma membrane, a phenomenon that was lost when cells were cultured under hyperglycemic (20 mM) conditions or pretreated with wortmannin. There was however, an increase in GLUT1 expression as well as a 3-fold increase in hexokinase III expression, which was increased to nearly 5-fold in the presence of insulin, in response to L-PGDS at 20 mM glucose. In addition, adipocytes isolated from L-PGDS knockout mice were significantly less sensitive to insulin-stimulated glucose transport than wild-type. We conclude that L-PGDS, via production of prostaglandin D-2, is an important mediator of muscle and adipose glucose transport which is modulated by glycemic conditions and plays a significant role in the glucose intolerance associated with type 2 diabetes. (C) 2008 Elsevier Inc. All rights reserved.
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