Mammalian preimplantation blastocysts exhibit insulin-stimulated glucose uptake despite the absence of the only known insulinregulated transporter, GLUT4. We describe a previously unidentified member of the mammalian facilitative GLUT superfamily that exhibits Ϸ20 -25% identity with other murine facilitative GLUTs. Insulin induces a change in the intracellular localization of this protein, which translates into increased glucose uptake into the blastocyst, a process that is inhibited by antisense oligoprobes. Presence of this transporter may be necessary for successful blastocyst development, fuel metabolism, and subsequent implantation. Moreover, the existence of an alternative transporter may explain examples in other tissues of insulin-regulated glucose transport in the absence of GLUT4.
Cynanchum wilfordii is used in traditional Chinese medicine with almost all parts of this plant considered beneficial for various vascular diseases. This study was performed to evaluate the effect of an ethanol extract of C. wilfordii (ECW) on vascular dysfunction in apolipoprotein E (apoE)(-/-) mice fed with high fat/cholesterol diets (HFCDs). The apoE(-/-) mice were fed HFCD consisting of 7.5% cocoa butter and 1.25% cholesterol, with or without 100 or 200 mg/day/kg ECW. Chronic ECW treatment significantly lessened the level of low-density lipoprotein (P<.05) and elevated that of high-density lipoprotein-cholesterol (P<.01). Chronic ECW treatment normalized the HFCD-induced increase in systolic blood pressure, maintained smooth and soft intimal endothelial layers, and decreased intima-media thickness in aortic sections of HFCD-fed apoE(-/-) mice. ECW significantly restored the diet-induced decrease in vasorelaxation response to acetylcholine; however, the response to sodium nitroprusside did not change. ECW clearly restored the HFCD-induced reduction in endothelial nitric oxide synthase expression levels in aortic tissue, leading to decreased vascular inflammation through an inhibition of cellular adhesion molecules such as E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1 as well as endothelin-1 (ET-1) expression. In conclusion, ECW ameliorates endothelial dysfunction via improvement of the nitric oxide/cyclic GMP signaling pathway in a diet/genetic model of hyperlipidemia. ECW also substantially inhibited the development of atherosclerosis, possibly by inhibiting ET-1, cell adhesion molecules, and lesion formation, suggesting a vascular protective role for this herb in the treatment and prevention of atherosclerotic vascular disease.
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