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Metforminium Decavanadate (MetfDeca) Treatment Ameliorates Hippocampal Neurodegeneration and Recognition Memory in a Metabolic Syndrome Model

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Abstract

The consumption of foods rich in carbohydrates, saturated fat, and sodium, accompanied by a sedentary routine, are factors that contribute to the progress of metabolic syndrome (MS). In this way, they cause the accumulation of body fat, hypertension, dyslipidemia, and hyperglycemia. Additionally, MS has been shown to cause oxidative stress, inflammation, and death of neurons in the hippocampus. Consequently, spatial and recognition memory is affected. It has recently been proposed that metformin decavanadate (MetfDeca) exerts insulin mimetic effects that enhance metabolism in MS animals; however, what effects it can cause on the hippocampal neurons of rats with MS are unknown. The objective of the work was to evaluate the effect of MetfDeca on hippocampal neurodegeneration and recognition memory in rats with MS. Administration of MetfDeca for 60 days in MS rats improved object recognition memory (NORt). In addition, MetfDeca reduced markers of oxidative stress and hippocampal neuroinflammation. Accompanied by an increase in the density and length of the dendritic spines of the hippocampus of rats with MS. We conclude that MetfDeca represents an important therapeutic agent to treat MS and induce neuronal and cognitive restoration mechanisms.

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Availability of Data

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Acknowledgements

We want to thank Dr. Francisco Ramos for his help with the animal care. Thanks to Professor Thomas Edwards PhD., for editing the English language text.

Funding

Funding for this study was provided by grants from VIEP-BUAP Grant (No. DIFA-NAT19-G) to DA and ST, (No. TEMS-NAT19-I) to TS and PAPIIT-UNAM (IN214117) to JG. None of the funding institutions had any further role in the study design, the collection of data, analyses, and interpretation of data, writing of the report or in the decision to submit the paper for publication and interpretation of data, writing of the report or the decision to submit the paper for publication.

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Authors and Affiliations

  1. Faculty of Chemical Sciences, Benemerita Autonomous University of Puebla, Puebla, Pue, Mexico

    Alfonso Diaz, Guadalupe Muñoz-Arenas & Samuel Treviño

  2. Faculty of Biological Sciences, Benemerita Autonomous University of Puebla, Puebla, Pue, Mexico

    Berenice Venegas

  3. Laboratory of Neuropsychiatry, Institute of Physiology, Benemerita Autonomous University of Puebla, Puebla, Pue, Mexico

    Rubén Vázquez-Roque & Gonzalo Flores

  4. Department of Biochemistry, Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico

    Jorge Guevara

  5. Chemistry Center, ICUAP, Benemerita Autonomous University of Puebla, Puebla, Pue, Mexico

    Enrique Gonzalez-Vergara

Authors
  1. Alfonso Diaz
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  2. Guadalupe Muñoz-Arenas
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  3. Berenice Venegas
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  4. Rubén Vázquez-Roque
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  5. Gonzalo Flores
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  6. Jorge Guevara
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  7. Enrique Gonzalez-Vergara
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  8. Samuel Treviño
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Contributions

AD and ST designed the study and wrote the protocol. AD, BV, GMA, and RVR performed the experiments. AD, ST, EGV, GF, and JG managed the literature searches and analysis, EGV undertook the statistical analysis. AD and ST wrote the first draft of the manuscript. All contributing authors have approved the final manuscript.

Corresponding author

Correspondence to Samuel Treviño.

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Diaz, A., Muñoz-Arenas, G., Venegas, B. et al. Metforminium Decavanadate (MetfDeca) Treatment Ameliorates Hippocampal Neurodegeneration and Recognition Memory in a Metabolic Syndrome Model. Neurochem Res 46, 1151–1165 (2021). https://doi.org/10.1007/s11064-021-03250-z

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  • DOI: https://doi.org/10.1007/s11064-021-03250-z

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