Vanadyl Sulfate Does Not Enhance Insulin Action in Patients With Type 1 Diabetes

Aharon, Yigal; Mevorach, Michèle; Shamoon, Harry

doi:10.2337/diacare.21.12.2194

Cited by 10 publications

(4 citation statements)

References 3 publications

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“…The concentrations of vanadate used in this study are compatible with what has been observed in plasma after chronic treatment with vanadate (50-90 M) in animals and in humans (1,47). This is in contrast to the acute action of this compound, when millimolar concentrations of vanadate are required to produce an effect in vitro (11,19,20,31,41,43).…”

Section: Discussionsupporting

confidence: 57%

Stimulation of glucose uptake by chronic vanadate pretreatment in cardiomyocytes requires PI 3-kinase and p38 MAPK activation

Tardif

Julien

Chiasson

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Coderre. Stimulation of glucose uptake by chronic vanadate pretreatment in cardiomyocytes requires PI 3-kinase and p38 MAPK activation. Am J Physiol Endocrinol Metab 284: E1055-E1064, 2003. First published December 10, 2002 10.1152 10. /ajpendo.00134.2002 inhibitor of tyrosine phosphatases, has insulin-mimetic properties. It has been shown that acute vanadate administration enhances glucose uptake independently of phosphatidylinositol (PI) 3-kinase and p38 MAPK. However, therapeutic vanadate use requires chronic administration, and this could potentially involve a different signaling pathway(s). Thus, we examined the mechanisms by which chronic vanadate exposure (16 h) stimulates glucose uptake in primary cultures of adult cardiomyocytes. The effect of vanadate on the activation of insulin-signaling molecules was evaluated 60 min after its withdrawal and in the absence of insulin. We therefore evaluated the persistent effect of vanadate on the insulin-signaling cascade. Our results demonstrate that preincubation with low vanadate concentrations (25-75 M) induces a dose-dependent increase in glucose uptake. The augmentation of this process was not due to alterations in GLUT1 or GLUT4 protein levels, transcription, or de novo protein synthesis. Chronic vanadate exposure was associated with activation of the insulin receptor, insulin receptor substrate-1 (IRS-1), PKB/Akt, and p38 MAPK. Furthermore, inhibition of PI 3-kinase or p38 MAPK by wortmannin and PD-169316, respectively, significantly inhibited vanadate-mediated glucose uptake in cardiomyocytes. Thus, over time, different (albeit overlapping) signaling cascades may be activated by vanadate. insulin signaling; protein kinase B/Akt; diabetes; vanadium; heart; phosphatidylinositol 3-kinase DESPITE THE ABILITY OF THE HEART to use multiple substrates to meet its energy requirements, this organ has one of the highest rates of glucose utilization in vivo (18,45). Decreased glucose uptake has been observed in both type 1 and type 2 diabetic subjects (25,29,45), and it has been proposed that abnormal regulation of this process has a role in the development of cardiac dysfunction (13). In db/db mice, a model of type 2 diabetes characterized by a reduction in glucose utilization and myocardial dysfunction, selective overexpression of the major glucose transporter GLUT4 expressed in the heart normalized these abnormalities (4). Interestingly, vanadate administration to streptozotocin-induced diabetic rats improved both insulin action and myocardial function in these animals (49). Furthermore, it has been shown that chronic vanadate exposure augments glucose uptake and improves ischemic tolerance in the hypertrophied heart (41). Together, these data suggest that glucose is an important cardiac substrate and that vanadate, by stimulating glucose uptake, could have a beneficial effect on the diabetic heart.Vanadium is a trace element found in most cells in concentrations ranging from 0.1 to 1 M (31). Vanadium compounds, such as vanadate, are inhibitors of protein tyrosine...

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Section: Discussionsupporting

confidence: 57%

Stimulation of glucose uptake by chronic vanadate pretreatment in cardiomyocytes requires PI 3-kinase and p38 MAPK activation

Tardif

Julien

Chiasson

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…In type 1 diabetes patients, oral administration of sodium metavanadate and vanadyl sulfate in doses of 50–125 mg/day during 2 to 4 weeks, improves fasting plasma glucose levels and daily insulin requirements in type 1 diabetic patients. Similar doses administrated to type 2 diabetes subjects showed an increase in insulin sensitivity, reduction in fasting plasma glucose levels and glycosylated hemoglobin (HbA 1c ), and alleviation insulin resistance, besides suppressing endogenous hepatic glucose production [45, 268, 269, 288–291].…”

Section: Vanadium Signal Transduction Cascades and Therapeutic Implicmentioning

confidence: 99%

Vanadium in Biological Action: Chemical, Pharmacological Aspects, and Metabolic Implications in Diabetes Mellitus

Treviño

Díaz

Sánchez-Lara

et al. 2018

Biol Trace Elem Res

241

126

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Vanadium compounds have been primarily investigated as potential therapeutic agents for the treatment of various major health issues, including cancer, atherosclerosis, and diabetes. The translation of vanadium-based compounds into clinical trials and ultimately into disease treatments remains hampered by the absence of a basic pharmacological and metabolic comprehension of such compounds. In this review, we examine the development of vanadium-containing compounds in biological systems regarding the role of the physiological environment, dosage, intracellular interactions, metabolic transformations, modulation of signaling pathways, toxicology, and transport and tissue distribution as well as therapeutic implications. From our point of view, the toxicological and pharmacological aspects in animal models and humans are not understood completely, and thus, we introduced them in a physiological environment and dosage context. Different transport proteins in blood plasma and mechanistic transport determinants are discussed. Furthermore, an overview of different vanadium species and the role of physiological factors (i.e., pH, redox conditions, concentration, and so on) are considered. Mechanistic specifications about different signaling pathways are discussed, particularly the phosphatases and kinases that are modulated dynamically by vanadium compounds because until now, the focus only has been on protein tyrosine phosphatase 1B as a vanadium target. Particular emphasis is laid on the therapeutic ability of vanadium-based compounds and their role for the treatment of diabetes mellitus, specifically on that of vanadate-and polioxovanadate-containing compounds. We aim at shedding light on the prevailing gaps between primary scientific data and information from animal models and human studies.

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“…The commonly employed inorganic vanadium salts include vanadyl sulphate, orthovanadate and metavanadate [11,15,16,[18][19][20][21][22][23][24]. These vanadium compounds are used in experimental diabetes induced in animals [4,11,18,21,22,24,25] as well as in human diabetic volunteers [15,16,19,20,23,26,27]. Although the physiological and biochemical influence of these vanadium complexes on the organism, organ or tissue level is very well known, their molecular mechanism and effect on intracellular organelle is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…Among them, vanadium derivatives both organic [1][2][3][4][5][6][7][8][9][10] and inorganic [10][11][12][13][14][15][16][17][18] are very effective, however, they show some side effect. The commonly employed inorganic vanadium salts include vanadyl sulphate, orthovanadate and metavanadate [11,15,16,[18][19][20][21][22][23][24]. These vanadium compounds are used in experimental diabetes induced in animals [4,11,18,21,22,24,25] as well as in human diabetic volunteers [15,16,19,20,23,26,27].…”

Section: Introductionmentioning

confidence: 99%

Sodium orthovanadate exerts influence on liver Golgi complexes from control and streptozotocin-diabetic rats

Kordowiak

Goc

Drozdowska

et al. 2005

Journal of Inorganic Biochemistry

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Vanadyl Sulfate Does Not Enhance Insulin Action in Patients With Type 1 Diabetes

Cited by 10 publications

References 3 publications

Stimulation of glucose uptake by chronic vanadate pretreatment in cardiomyocytes requires PI 3-kinase and p38 MAPK activation

Stimulation of glucose uptake by chronic vanadate pretreatment in cardiomyocytes requires PI 3-kinase and p38 MAPK activation

Vanadium in Biological Action: Chemical, Pharmacological Aspects, and Metabolic Implications in Diabetes Mellitus

Sodium orthovanadate exerts influence on liver Golgi complexes from control and streptozotocin-diabetic rats

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