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

Oxidative Medicine and Cellular Longevity - Tập 2016 Số 1 - 2016
Samuel Treviño1,2, Denisse Velázquez-Vázquez2, Eduardo Sánchez‐Lara3, Alfonso Díaz4, José Ángel Flores-Hernández1, Aarón Pérez-Benı́tez5, Eduardo Brambila-Colombres1,2, Enrique González‐Vergara3
1Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 18 Sur y Avenida San Claudio, Colonia San Manuel, 72570 Puebla, PUE, Mexico
2Laboratorio de Investigación en Química Clínica, Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 18 Sur y Avenida San Claudio, Colonia San Manuel, 72570 Puebla, PUE, Mexico
3Laboratorio de Bioinorgánica Aplicada, Centro de Química ICUAP, Benemérita Universidad Autónoma de Puebla, 18 Sur y Avenida San Claudio, Colonia San Manuel, 72570 Puebla, PUE, Mexico
4Departamento de Farmacia, Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 18 Sur y Avenida San Claudio, Colonia San Manuel, 72570 Puebla, PUE, Mexico
5Laboratorio de Nuevos Materiales, Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 18 Sur y Avenida San Claudio, Colonia San Manuel, 72570 Puebla, PUE, Mexico

Tóm tắt

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.

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Oxidative Medicine and Cellular Longevity

Tập 2016 Số 1

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