Effect of valproic acid, trichostatin A and resveratrol in adipocyte differentiation

Efecto del ácido valproico, tricostatin A y resveratrol sobre la diferenciación del adipocito

Published 2009-06-30

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Effect of valproic acid, trichostatin A and resveratrol in adipocyte differentiation. (2009). NOVA, 7(11). https://doi.org/10.22490/24629448.413
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Johana Brochero
    Diana Vargas
      Carolina Romero
        Luis Gustavo Celis
          Fernando Lizcano
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            Obesity is a risk factor of coronary diseases, cancer, vascular brain disorders, and diabetes type II. The purpose of this work is to evaluate the capacity of valproic acid, trichostatin A and resveratrol agents in the reduction of fat accumulation in the adipocyte cell. Valproic acid and trichostatin A inhibit histone deacetilase activity type I and II, while resveratrol is a sirtuin 1 activator belonging to the family of nicotinamide dinucleotids-dependent deacetylases histones. Furthermore, Sirt1 represses the activity mediated by PPAR γ by means of its association with repressors, showed in the mobilization of fatty acids in adipocyte cells. For this study, mouse preadipocytes 3T3-L1 cell line was used and treated it in the presence of a differentiation cocktail containing rosiglitazone, isobutilmetilxantine and dexametasone. In the 8th day of differentiation doses of  valproic acid, trichostatin and resveratrol were added, monitoring each two days until day 12 of differentiation. The fat storage by oil red-O solution was evaluated assessing the triglyceride quantity in each treatment. All the treatments presented a reduction in the adipocyte differentiation, because the amount of triglycerides was lower in comparison to the cells differentiated by rosiglitazone. However, the resveratrol presented a greater meaningful difference. Overall our results highlight a role for HDAC and Sirt1 activity in adipogenesis, which can be blocked by treatment with valproic acid, trichostatin A and resveratrol, being resveratrol the agent that presents the greatest reduction in adipocyte differentiation.

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            17. DOI: http://dx.doi.org/10.22490/24629448.413
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