Vanadyl Sulfate via Glut-4 transcription or not???

[Drveejay11]

The literature seems to be inconclusive. The reason I ask is I am trying to utilize ALA, vinegar, and VAnadyl Sulfate for optimimim glucose disposal. I believe they work via different mediations.

My concern, if Vanadyl does NOT act as a Glut-4 transcriptor/mediator, and ONLY acts to increase insulin sensitivity......it becomes a NON-Indicated product for fatty meals....very important to figure out here.

I usually use ALA and vinegar for "Carb-UP and Pig-out meals". This may not be a good idea with Vanadium.

Anyone????

 

[natty]

I know Vanadyl Sulfate is toxic at a relatively low dose so I dont know that it would be a good idea... but ive also read studies which showed it really doesnt work all that well in comparison to ALA.

 

[Drveejay11]

I hear ya on the "toxicity" issue. It's over-rated IMO! And most of you know I tend to favor the conservative side of controversial substances.

I do NOT believe from all my reading thus far that Vanadyl Sulfate is the beast it is being played out to be. It's reputation is somewhat similar to B-3........Tauted as "highly liver toxic"........therefore its vast and most pronounced beneficial effects are put aside (a potent insulin mimicker).

I just don't but it! At least not to the degree it's been played at.

Vanadium HAS its place IMO......as does Taurine/vinegar (acetic acid), and selenium selenate, and ALA in regards to proper glucose transport and disposal.

I find it OUTRAGEOUS that more bro's on this board shy away from things such as Vanayl Sulfate but aren't too quick dismiss the potential harm the POWERFUL hormone insulin can inflict! (and I'm NOT talking about acutely........but chronically--------Syndrome "X").

Now answer the original question damn it! I know your intelligent ass knows the answer! QUIT holding out on me ..... LOL

 

[natty]

Vanadyl sulfate-stimulated glycogen synthesis is associated with activation of phosphatidylinositol 3-kinase and is independent of insulin receptor tyrosine phosphorylation.
Biochemistry 1998 May 12;37(19):7006-14 (ISSN: 0006-2960)
Pandey SK; Anand-Srivastava MB; Srivastava AK
Centre de Recherche, Centre Hospitalier Universite de Montreal, Quebec, Canada.
Salts of the trace element vanadium, such as sodium orthovanadate and vanadyl sulfate (VS), exhibit a myriad of insulin-like effects, including stimulation of glycogen synthesis and improvement of glucose homeostasis in type I and type II animal models of diabetes mellitus. However, the cellular mechanism by which these effects are mediated remains poorly characterized. We have shown earlier that different vanadium salts stimulate the MAP kinase pathway and ribosomal-S-6-kinase (p70s6k) in chinese hamster ovary cells overexpressing human insulin receptor (CHO-HIR cells) [Pandey, S. K., Chiasson, J.-L., and Srivastava, A. K. (1995) Mol. Cell. Biochem. 153, 69-78]. In the present studies, we have investigated if similar to insulin, VS also activates phosphatidylinositol 3-kinase (PI3-k) activity, and whether VS-induced activation of the PI3-k, MAP kinase, and p70s6k pathways contributes to glycogen synthesis. Treatment of CHO-HIR cells with VS resulted in increased glycogen synthesis and PI3-k activity which were blocked by pretreatment of the cells with wortmannin and LY294002, two specific inhibitors of PI3-k. On the other hand, PD98059 and rapamycin, specific inhibitors of the MAP kinase pathway and p70s6k, respectively, were unable to inhibit VS-stimulated glycogen synthesis. Moreover, VS-stimulated glycogen synthesis and PI3-k were observed without any change in the tyrosine phosphorylation of insulin receptor (IR) beta-subunit but were associated with increased tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1). In addition, PI3-k activation was detected in IRS-1 immunoprecipitates from VS-stimulated cells, indicating that tyrosine-phosphorylated IRS-1 was able to interact and thereby activate PI3-k in response to VS. Taken together, these results provide evidence that tyrosine phosphorylation of IRS-1 and activation of PI3-k play a key role in mediating the insulinomimetic effect of VS on glycogen synthesis independent of IR-tyrosine phosphorylation.

 

[Drveejay11]

God Bless ya