Lack of in vivo effect of vanadium on GLUT4 translocation in white adiposetissue of streptozotocin-diabetic rats

Citation
Mc. Cam et al., Lack of in vivo effect of vanadium on GLUT4 translocation in white adiposetissue of streptozotocin-diabetic rats, METABOLISM, 50(6), 2001, pp. 674-680
Citations number
34
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
METABOLISM-CLINICAL AND EXPERIMENTAL
ISSN journal
00260495 → ACNP
Volume
50
Issue
6
Year of publication
2001
Pages
674 - 680
Database
ISI
SICI code
0026-0495(200106)50:6<674:LOIVEO>2.0.ZU;2-E
Abstract
Vanadium treatment, in vivo, corrects the severe hyperglycemia observed in streptozotocin (STZ)-diabetic rats. A number of metabolic effects of vanadi um have been demonstrated in vitro and might contribute importantly to norm alization of glucose homeostasis. However, many in vitro effects of vanadiu m occur at concentrations substantially higher than those achieved in vivo. Effects of vanadium on white adipose tissue have been particularly well ch aracterized in vitro. To examine the relationship between in vitro and in v ivo actions of vanadium, we examined the effects of vanadium treatment on a cute glucose tolerance and adipose tissue GLUT4 control in vivo. In agreeme nt with previous studies, vanadium treatment of STZ-diabetic rats restored normoglycemia with no appreciable restoration of insulin secretion. GLUT4 e xpression in white adipose tissue was reduced by 22% in STZ-diabetic rats c ompared with controls. Vanadium treatment did not significantly alter GLUT4 expression in controls, but completely restored normal expression levels i n STZ-diabetic rats. In overnight-fasted control animals, GLUT4 translocati on to the plasma membrane (PM) was maximally elevated (by 50%) in adipose t issue within 5 to 10 minutes after an intravenous (IV) glucose challenge. N o glucose-induced translocation of GLUT4 was detected in diabetic rats, and peak PM GLUT4 content was 40% lower than in controls. Vanadium treatment d id not increase peak PM GLUT4 content in either control or diabetic animals in response to a glucose load. Finally, the suppression of whole-body acut e glucose tolerance in diabetic animals was only partially normalized by va nadium treatment. We conclude: (1) that concentrations of vanadium effectiv e for maintaining normoglycemia in vivo (typically below 30 mu mol/L) promo te normal GLUT4 expression, but do not influence the subcellular localizati on of GLUT4 in white adipose tissue and (2) that in vivo effects of vanadiu m may not necessarily reflect the actions observed in vitro at supraphysiol ogic concentrations. Copyright (C) 2001 by W.B, Saunders Company.