Skip to main navigation menu Skip to main content Skip to site footer

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

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




Section
Artículo Original

How to Cite
Brochero, J., Vargas, D., Romero, C., Celis, L. G., & Lizcano, F. (2009). Effect of valproic acid, trichostatin A and resveratrol in adipocyte differentiation. NOVA, 7(11). https://doi.org/10.22490/24629448.413

Dimensions
PlumX
license

Licencia Creative Commons

NOVA by http://www.unicolmayor.edu.co/publicaciones/index.php/nova is distributed under a license creative commons non comertial-atribution-withoutderive 4.0 international.

Furthermore, the authors keep their property intellectual rights over the articles.

 

Johana Brochero
    Diana Vargas
      Carolina Romero
        Luis Gustavo Celis
          Fernando Lizcano

            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.

            Article visits 146 | PDF visits 90


            Downloads

            Download data is not yet available.
            1. Fu M, Sun T, Bookout AL, Downes M, Yu RT, Evans RM, Mangelsdorf DJ. A Nuclear Receptor Atlas: 3T3-L1 Adipogenesis. Mol Endocrinol. 2005; 19:2437-2450.
            2. Macritchie KA, Geddes JR, Scott J, Haslam DR, Goodwin GM. Valproic acid, valproate and divalproex in the maintenance treatment of bipolar disorder. Cochrane Database Syst Rev. 2001;3:CD003196.
            3. Jallon P, Picard F. Bodyweight Gain and Anticonvulsants: A Comparative Review. Drug Saf. 2001;24:969–978.
            4. Lagace DC, Nachtigal MW. Inhibition of histone deacetylase activity by valproic acid blocks adipogenesis. J Biol Chem. 2004;279:18851–18860.
            5. Vanhaecke T, Papeleu P, Elaut G, Rogiers V. Trichostatin A-like hydroxamate histone deacetylase inhibitors as therapeutic agents: toxicological point of view. Curr Med Chem 2004;11:1629-1643.
            6. Drummond DC, Noble CO, Kirpotin DB, Guo Z, Scott GK, Benz CC. Clinical development of histone deacetylase inhibitors as anticancer agents. Annu Rev Pharmacol Toxicol. 2005;45:495-528.
            7. Shankar S, Srivastava RK. Histone deacetylase inhibitors: mechanisms and clinical significance in cancer: HDAC inhibitor-induced apoptosis. Adv Exp Med Biol. 2008;615:261-298.
            8. Baur JA, Sinclair D. Therapeutic potencial of resveratrol: the in vivo evidence. Nat Rev Drug Discov. 2006;5:493-566.
            9. Sauve AA, Wolberger C, Schramm VL, Boeke JD. The biochemistry of sirtuins. Annu Rev Biochem. 2006;75:435-465.
            10. Alkhalaf M. Resveratrol-induced growth inhibition in MDAMB- 231 breast cancer cells is associated with mitogen-activated protein kinasa signalling and protein translation. Eur J Cancer Prev. 2007;16:334-341.
            11. Picard F, Kurtev M, Chung N, Topark-Ngarm A, Senawong T, Machado De Oliveira R, Leid M, et al. Sirt1 promotes fat mobilization in white adipocytes by repressing PPARg. Nature. 2004; 429:771-776.
            12. Kasturi R, Joshi VC. Hormonal Regulation of Stearoyl Coenzyme A Desaturase Activity and Lipogenesis during Adipose Conversionof 3T3-Ll Cells. J Biol Chem. 1982;257:12224-12230.
            13. Celis LG, Rozo C, Garay J, Vargas D, Lizcano F. Efecto Lipolítico del Resveratrol en células 3T3-L1. Salud Uninorte. 2008;24:165-171
            14. Puigserver P, Wu Z, Park CW, Graves R, Wright M, Spiegelman BM. A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis. Cell. 1998;92:829–839.
            15. Lagouge M, Argmann C, Gerhart-Hines Z, Meziane H, Lerin C, Daussin F, Messadeq N, et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell. 2006;127:1109-1122
            16. -------------------------------------------------------------------------------
            17. DOI: http://dx.doi.org/10.22490/24629448.413
            Sistema OJS 3.4.0.5 - Metabiblioteca |