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. 2016;2016:6058705.
doi: 10.1155/2016/6058705. Epub 2016 Mar 28.

Metforminium Decavanadate as a Potential Metallopharmaceutical Drug for the Treatment of Diabetes Mellitus

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Free PMC article

Metforminium Decavanadate as a Potential Metallopharmaceutical Drug for the Treatment of Diabetes Mellitus

Samuel Treviño et al. Oxid Med Cell Longev. .
Free PMC article

Abstract

New potential drugs based on vanadium are being developed as possible treatments for diabetes mellitus (DM) and its complications. In this regard, our working group developed metforminium decavanadate (MetfDeca), a compound with hypoglycemic and hypolipidemic properties. MetfDeca was evaluated in models of type 1 and type 2 diabetes mellitus, on male Wistar rats. Alloxan-induction was employed to produce DM1 model, while a hypercaloric-diet was employed to generate DM2 model. Two-month treatments with 3.7 μg (2.5 μM)/300 g/twice a week for DM2 and 7.18 μg (4.8 μM)/300 g/twice a week for DM1 of MetfDeca, respectively, were administered. The resulting pharmacological data showed nontoxicological effects on liver and kidney. At the same time, MetfDeca showed an improvement of carbohydrates and lipids in tissues and serum. MetfDeca treatment was better than the monotherapies with metformin for DM2 and insulin for DM1. Additionally, MetfDeca showed a protective effect on pancreatic beta cells of DM1 rats, suggesting a possible regeneration of these cells, since they recovered their insulin levels. Therefore, MetfDeca could be considered not only as an insulin-mimetic agent, but also as an insulin-enhancing agent. Efforts to elucidate the mechanism of action of this compound are now in progress.

Figures

Figure 1
Figure 1
Ball and stick representation of metforminium decavanadate (H2Metf)3[V10O28]·8H2O. Water molecules are omitted for clarity [11].
Figure 2
Figure 2
Administration of MetfDeca showing a lowering in blood glucose levels of hyperglycemic rats. The animals (n = 10/group) were administered with this compound at doses (0.7, 1.4, 2.5, 5, and 10 μM) for 4 weeks in rats with alloxan-induced hyperglycemia (150 mg/kg). The graph shows the percentage of animals with reduced levels of glucose.
Figure 3
Figure 3
Oral glucose tolerance, insulin response, and fraction A1c of the glycosylated hemoglobin in different groups to two months of treatment. (a–c) Independent insulin (I-I) model. (d–f) Insulin-requiring (I-R) model. The results shown are the average of 5 different experiments ± SEM. indicates significant difference from the control group p ≤ 0.05 group by ANOVA test with a Bonferroni post hoc test.
Figure 4
Figure 4
Glycogen content in different tissues from groups to two months with treatments. (a–d) Independent insulin (I-I) model. (e–h) Insulin-requiring (I-R) model. The results shown are the average of 20 different experiments ± SEM. indicates significant difference above from the control group (NC); meanwhile ▼ indicates significant difference below from the control group (NC), both with p ≤ 0.05 group by ANOVA test with a Bonferroni post hoc test.
Figure 5
Figure 5
Triglyceride content in different tissues from groups to two months with treatments. (a–d) Independent insulin (I-I) model. (e–h) Insulin-requiring (I-R) model. The results shown are the average of 20 different experiments ± SEM. indicates significant difference above from the control group (NC); meanwhile ▼ indicates significant difference below from the control group (NC), both with p ≤ 0.05 group by ANOVA test with a Bonferroni post hoc test.

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