Vanadate inhibits glucose output from isolated perfused rat liver

Bruck, R.

doi:10.1016/0270-9139(91)90196-3

Cited by 6 publications

(6 citation statements)

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“…In groups with LPS, similar to groups without LPS in time-dependent manner, levels of ALT and AST increased at AFB1 concentrations of 0.01, 0.1 and 1 ppm, that concentrations of 0.1 and 1ppm had statistically significant different with LPS group. Our finding is consistent with the most investigators finding about time course of enzyme changes in exposure with naproxen [15], copper and AFB1 [16][17][18], cadmium [19], vanadium [20] in perfused rat liver model.…”

Section: Discussionsupporting

confidence: 93%

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Koohi

Staji

Hayati

et al. 2017

IJT

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Section: Discussionsupporting

confidence: 93%

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Koohi

Staji

Hayati

et al. 2017

IJT

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“…In vitro vanadate mimics many of the actions of insulin in freshly isolated cells and target tissues as well as in cultured cells (15)(16)(17)(18). During such studies we found that exposure of cultured human lymphocytes (IM-9) to vanadate resulted in a decrease in the number of cell-surface insulin receptors (19) similar to that previously described for insulin (20).…”

supporting

confidence: 60%

The Insulin-Mimetic Agent Vanadate Promotes Receptor Endocytosis and Inhibits Intracellular Ligand-Receptor Degradation by a Mechanism Distinct From the Lysosomotropic Agents

Fantus

George²,

Tang³

et al. 1996

Diabetes

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Vanadate (sodium orthovanadate) is an insulin-mimetic agent and phosphotyrosine phosphatase inhibitor that has been proposed as a potential therapeutic agent for diabetes. We previously reported that vanadate decreased the number of cell-surface insulin receptors but inhibited receptor degradation in cultured lymphocytes (IM-9) (1). To determine whether vanadate affected receptors without intrinsic tyrosine kinase activity, its effects on LDL and transferrin receptors and their ligands were examined. Vanadate exposure resulted in a dose- and time-dependent decrease in LDL binding to cultured human fibroblasts associated with a decrease in cell surface receptor number while total solubilized cell LDL receptors increased. Vanadate also inhibited the LDL-mediated downregulation of total cellular LDL receptors in the absence and presence of cycloheximide consistent with an inhibition of LDL receptor degradation. In the case of the ligand, vanadate augmented the accumulation of intact 125I-LDL associated with an inhibition of up to 80% of the ability of LDL to decrease cholesterol synthesis. Since these actions were similar to the effects of lysosomotropic agents, we examined the effect of vanadate on intraendosomal pH using the fluorescent probe acridine orange. In contrast with chloroquine and NH4Cl, vanadate did not neutralize the pH of the acidic intracellular compartment. Furthermore, after a transient insulin-like effect, chronic exposure to vanadate diminished 125I-diferric transferrin binding to rat adipocytes. In contrast with the inhibitory action of NH4Cl, intracellular 59Fe uptake remained unaffected and was proportional to cell-surface binding capacity in the presence of vanadate. These data demonstrate a chronic effect of vanadate to promote the accumulation of intracellular receptors and to inhibit ligand and receptor degradation. The latter effect is not mediated by pH changes, appears to be localized to a late endosomal/lysosomal compartment, and suggests a possible role for tyrosine dephosphorylation in the regulation of receptor-ligand degradation.

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“…Glucose uptake and metabolism are stimulated in fat and muscle tissue (29,30), lipolysis is inhibited (31), and hepatic glucose output is suppressed (32,33). Oral administration of vanadate and vandyl resulted in lowering of glucose concentrations in rodent models of both type 1 and type 2 diabetes (34 -37).…”

mentioning

confidence: 99%

Enhanced Sensitivity of Insulin-resistant Adipocytes to Vanadate Is Associated with Oxidative Stress and Decreased Reduction of Vanadate (+5) to Vanadyl (+4)

Ennis²,

Lai

et al. 2001

Journal of Biological Chemistry

104

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Vanadate (sodium orthovanadate), an inhibitor of phosphotyrosine phosphatases (PTPs), mimics many of the metabolic actions of insulin in vitro and in vivo. The potential of vanadate to stimulate glucose transport independent of the early steps in insulin signaling prompted us to test its effectiveness in an in vitro model of insulin resistance. In primary rat adipocytes cultured for 18 h in the presence of high glucose (15 mM) and insulin (10 ؊7 M), sensitivity to insulin-stimulated glucose transport was decreased. In contrast, there was a paradoxical enhanced sensitivity to vanadate of the insulinresistant cells (EC 50 for control, 325 ؎ 7.5 M; EC 50 for insulin-resistant, 171 ؎ 32 M; p < 0.002). Enhanced sensitivity was also present for vanadate stimulation of insulin receptor kinase activity and autophosphorylation and Akt/protein kinase B Ser-473 phosphorylation consistent with more effective PTP inhibition in the resistant cells. Investigation of this phenomenon revealed that 1) depletion of GSH with buthionine sulfoximine reproduced the enhanced sensitivity to vanadate while preincubation of resistant cells with N-acetylcysteine (NAC) prevented it, 2) intracellular GSH was decreased in resistant cells and normalized by NAC, 3) exposure to high glucose and insulin induced an increase in reactive oxygen species, which was prevented by NAC, 4) EPR (electron paramagnetic resonance) spectroscopy showed a decreased amount of vanadyl (؉4) in resistant and buthionine sulfoximine-treated cells, which correlated with decreased GSH and increased vanadate sensitivity, while total vanadium uptake was not altered, and 5) inhibition of recombinant PTP1B in vitro was more sensitive to vanadate (؉5) than vanadyl (؉4). In conclusion, the parodoxical increased sensitivity to vanadate in hyperglycemia-induced insulin resistant adipocytes is due to oxidative stress and decreased reduction of vanadate (؉5) to vanadyl (؉4). Thus, sensitivity of PTP inhibition and glucose transport to vanadate is regulated by cellular redox state.

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Vanadate inhibits glucose output from isolated perfused rat liver

Cited by 6 publications

References 0 publications

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

The Insulin-Mimetic Agent Vanadate Promotes Receptor Endocytosis and Inhibits Intracellular Ligand-Receptor Degradation by a Mechanism Distinct From the Lysosomotropic Agents

Enhanced Sensitivity of Insulin-resistant Adipocytes to Vanadate Is Associated with Oxidative Stress and Decreased Reduction of Vanadate (+5) to Vanadyl (+4)

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