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Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium.
Cell Biochem Biophys 2006; 44(1):73-81CB

Abstract

Among several metals, vanadium has emerged as an extremely potent agent with insulin-like properties. These insulin-like properties have been demonstrated in isolated cells, tissues, different animal models of type I and type II diabetes as well as a limited number of human subjects. Vanadium treatment has been found to improve abnormalities of carbohydrate and lipid metabolism and of gene expression in rodent models of diabetes. In isolated cells, it enhances glucose transport, glycogen and lipid synthesis, and inhibits gluconeogenesis and lipolysis. The molecular mechanism responsible for the insulin-like effects of vanadium compounds have been shown to involve the activation of several key components of insulin-signaling pathways that include the mitogen-activated-protein kinases (MAPKs) extracellular signal-regulated kinase 1/2 (ERK1/2) and p38MAPK, and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB). It is interesting that the vanadium effect on these signaling systems is independent of insulin receptor protein tyrosine kinase activity, but it is associated with enhanced tyrosine phosphorylation of insulin receptor substrate-1. These actions seem to be secondary to vanadium-induced inhibition of protein tyrosine phosphatases. Because MAPK and PI3-K/PKB pathways are implicated in mediating the mitogenic and metabolic effects of insulin, respectively, it is plausible that mimicry of these pathways by vanadium serves as a mechanism for its insulin-like responses.

Authors+Show Affiliations

Laboratory of Cell Signaling, Research Centre, Centre hospitalier de l'Université de Montréal-Hôtel-Dieu and Department of Medicine, Université de Montréal, Montreal, Quebec, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

16456236

Citation

Mehdi, Mohamad Z., et al. "Insulin Signal Mimicry as a Mechanism for the Insulin-like Effects of Vanadium." Cell Biochemistry and Biophysics, vol. 44, no. 1, 2006, pp. 73-81.
Mehdi MZ, Pandey SK, Théberge JF, et al. Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium. Cell Biochem Biophys. 2006;44(1):73-81.
Mehdi, M. Z., Pandey, S. K., Théberge, J. F., & Srivastava, A. K. (2006). Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium. Cell Biochemistry and Biophysics, 44(1), pp. 73-81.
Mehdi MZ, et al. Insulin Signal Mimicry as a Mechanism for the Insulin-like Effects of Vanadium. Cell Biochem Biophys. 2006;44(1):73-81. PubMed PMID: 16456236.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Insulin signal mimicry as a mechanism for the insulin-like effects of vanadium. AU - Mehdi,Mohamad Z, AU - Pandey,Sanjay K, AU - Théberge,Jean-François, AU - Srivastava,Ashok K, PY - 2006/2/4/pubmed PY - 2006/4/6/medline PY - 2006/2/4/entrez SP - 73 EP - 81 JF - Cell biochemistry and biophysics JO - Cell Biochem. Biophys. VL - 44 IS - 1 N2 - Among several metals, vanadium has emerged as an extremely potent agent with insulin-like properties. These insulin-like properties have been demonstrated in isolated cells, tissues, different animal models of type I and type II diabetes as well as a limited number of human subjects. Vanadium treatment has been found to improve abnormalities of carbohydrate and lipid metabolism and of gene expression in rodent models of diabetes. In isolated cells, it enhances glucose transport, glycogen and lipid synthesis, and inhibits gluconeogenesis and lipolysis. The molecular mechanism responsible for the insulin-like effects of vanadium compounds have been shown to involve the activation of several key components of insulin-signaling pathways that include the mitogen-activated-protein kinases (MAPKs) extracellular signal-regulated kinase 1/2 (ERK1/2) and p38MAPK, and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB). It is interesting that the vanadium effect on these signaling systems is independent of insulin receptor protein tyrosine kinase activity, but it is associated with enhanced tyrosine phosphorylation of insulin receptor substrate-1. These actions seem to be secondary to vanadium-induced inhibition of protein tyrosine phosphatases. Because MAPK and PI3-K/PKB pathways are implicated in mediating the mitogenic and metabolic effects of insulin, respectively, it is plausible that mimicry of these pathways by vanadium serves as a mechanism for its insulin-like responses. SN - 1085-9195 UR - https://www.unboundmedicine.com/medline/citation/16456236/Insulin_signal_mimicry_as_a_mechanism_for_the_insulin_like_effects_of_vanadium_ L2 - https://dx.doi.org/10.1385/CBB:44:1:073 DB - PRIME DP - Unbound Medicine ER -