Share This Article:

Effect of Caralluma Fimbriata Extract on 3T3-L1 Pre-Adipocyte Cell Division

Full-Text HTML Download Download as PDF (Size:1812KB) PP. 329-336
DOI: 10.4236/fns.2011.24047    5,651 Downloads   12,091 Views   Citations

ABSTRACT

A standardized extract of the plant Caralluma fimbriata (Slimaluma?) is widely used in the management of obesity but its mode of action is not yet clarified. This study investigated the ability of Caralluma fimbriata extract (CFE) to modify pre-adipocyte cell division and thus the development of hyper-plastic obesity. Mouse 3T3-L1 pre-adipocyte cell line samples were treated with different concentrations of an extract of CFE standardized against its pregnane glycoside content. Plain medium formed the negative control and hydroxyurea was the positive control. The cells were counted at 12-hour intervals, and their viability tested using the MTT assay. The treated cells were subjected to direct and indirect immunofluorescent assays for cyclin D1. CFE inhibited 3T3-L1 cell growth in a dose and duration-dependent manner, with results comparable to those produced by hydroxyurea. The viability of CFE-treated cells was reduced. Direct and indirect immunofluorescent assays demonstrated that CFE inhibits import of cyclin D1into the nucleus. CFE appears to inhibit pre-adipocyte cell division by interfering with a mechanism preceding the import of cyclin D1-CDk4/6 complex into the nucleus during the early G1 phase of the cell cycle, suggesting that CFE has the potential to inhibit hyperplastic obesity.

Cite this paper

S. Kamalakkannan, R. Rajendran, R. Venkatesh, P. Clayton and M. Akbarsha, "Effect of Caralluma Fimbriata Extract on 3T3-L1 Pre-Adipocyte Cell Division," Food and Nutrition Sciences, Vol. 2 No. 4, 2011, pp. 329-336. doi: 10.4236/fns.2011.24047.

References

[1] J. C. Seidell, “Epidemiology of Obesity,” Seminars in Vascular Medicine, Vol. 5, No. 1, February 2005, pp. 3-14. doi:10.1055/s-2005-871737
[2] E. E. Calle, C. Rodriguez, K. Walker-Thurmond and M. J. Thun, “Overweight, Obesity, and Mortality from Cancer in a Prospectively Studied Cohort of US Adults,” New England Journal of Medicine, Vol. 348, No. 17, April 2003, pp. 1625-1638. doi:10.1056/NEJMoa021423
[3] M. A. Beydoun, H. A. Beydoun and Y. Wang, “Obesity and Central Obesity as Risk Factors for Incident Dementia and Its Subtypes: A Systematic Review and Meta-Analysis,” Obesity Reviews, Vol. 9, No. 3, May 2008, pp. 204-218. doi:10.1111/j.1467-789X.2008.00473.x
[4] S. J. Olshansky, et al. “A Potential Decline in Life Expectancy in the United States in the 21st Century,” New England Journal of Medicine, Vol. 352, No. 11, March 2005, pp. 1138-1145. doi:10.1056/NEJMsr043743
[5] Q.-Q. Tang, T. C. Otto and M. D. Lane, “Mitotic Clonal Expansion: A Synchronous Process Required for Adipogenesis,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 100, No. 1, January 2003, pp. 44-49. doi:10.1073/pnas.0137044100
[6] C.-L. Hsu, S.-L. Huang and G.-C. Yen, “Inhibitory Effect of Phenolic Acids on the Proliferation of 3T3-L1 Preadipocytes in Relation to Their Antioxidant Activity,” Journal of Agricultural and Food Chemistry, Vol. 54, No. 12, June 2006, pp. 4191-4197. doi:10.1021/jf0609882
[7] P.-F. Hung, B.-T. Wu, et al., “Antimitogenic Effect of Green Tea (-)-Epigallocatechin Gallate on 3T3-L1 Preadipocytes Depends on the ERK and Cdk2 Pathways,” American Journal of Physiology, Cell Physiology, Vol. 288, No. 5, May 2005, pp. C1094-C1108. doi:10.1152/ajpcell.00569.2004
[8] J.-Y. Yang, et al., “Esculetin Induces Apoptosis and Inhibits Adipogenesis in 3T3-L1 Cells,” Obesity, Vol. 14, No. 10, October 2006, pp. 1691-1699. doi:10.1038/oby.2006.194
[9] D. Heber, “Herbal Preparations for Obesity: Are They Useful?” Primary Care: Clinics in Office Practice, Vol. 30, No. 2, June 2003, pp. 441-463. doi:10.1016/S0095-4543(03)00015-0
[10] M. H. Pittler, K. Schmidt and E. Ernst, “Adverse Events of herbal Food Supplements for Body Weight Reduction: Systematic Review,” Obesity Reviews, Vol. 6, No. 2, May 2005, pp. 93-111. doi:10.1111/j.1467-789X.2005.00169.x
[11] T. Lenz and W. Hamilton, “Supplemental Products Used for Weight Loss,” Journal of the American Pharmacists Association, Vol. 44, No. 1, January-February 2004, pp. 59-67. doi:10.1331/154434504322713246
[12] D. B. MacLean and L.-G. Luo, “Increased ATP Content/Production in the Hypothalamus May be a Signal for Energy-Sensing of Satiety: Studies of the Anorectic Mechanism of a Plant Steroidal Glycoside,” Brain Research, Vol. 1020, No. 1-2, September 2004, pp. 1-11. doi:10.1016/j.brainres.2004.04.041
[13] K. Ono, et al., “Intragastric Administration of Capsiate, a Transient Receptor Potential Channel Agonist, Triggers Thermogenic Sympathetic Responses,” Journal of Applied Physiology, Vol. 110, No. 3, March 2011, pp. 789- 798. doi:10.1152/japplphysiol.00128.2010
[14] Council of Scientific & Industrial Research, “Wealth of India: A Dictionary of Indian Raw Materials and Industrial Products,” Council of Scientific & Industrial Research, Delhi, 1985.
[15] J. C. Loudon, “Loudon’s Hortus Britannicus. A Catalogue of All the Plants, Indigenous, Cultivated in, or Introduced to Britain,” Brown and Green, London, 1830.
[16] E. Abdel-Sattar, M. R. Meselhy and M. A. Al-Yahya, “New Oxypregnane Glycosides from Caralluma Penicillata,” Planta Medica, Vol. 68, No. 5, May 2002, pp. 430-434. doi:10.1055/s-2002-32078
[17] H. Preuss, “Report on the Safety of Caralluma Fimbriata and Its Extract,” 2004. http://www.federalabs.com/analyses/Saftey%20of%20Caralluma.pdf
[18] R. Kuriyan, et al., “Effect of Caralluma Fimbriata Extract on Appetite, Food Intake and Anthropometry in Adult Indian Men and Women,” Appetite, Vol. 48, No. 3, May 2007, pp. 338-344. doi:10.1016/j.appet.2006.09.013
[19] S. Kamalakkannan, et al., “Anti-Obesogenic and Anti-Atherosclerotic Properties of Caralluma Fimbriata Extract,” 2010. http://www.ncbi.nlm.nih.gov/pubmed/21234320
[20] C. Zhang, et al., “Effect of Emodin on Proliferation and Differentiation of 3T3-L1 Preadipocyte and FAS Activity,” Chinese Medical Journal, Vol. 115, No. 7, July 2002, pp. 1035-1038.
[21] N. Hemati, et al., “Signaling Pathways through Which Insulin Regulates CCAAT/Enhancer Binding Protein α (C/EPBα) Phosphorylation and Gene Expression in 3T3- -L1 Adipocytes,” Journal of Biological Chemistry, Vol. 272, No. 41, October 1997, pp. 25913-25919. doi:10.1074/jbc.272.41.25913
[22] F. R. van Heerden, et al., “An Appetite Suppressant from Hoodia Species,” Phytochemistry, Vol. 68, No. 20, October 2007, pp. 2545-2553. doi:10.1016/j.phytochem.2007.05.022
[23] T. Mosmann, “Rapid Colorimetric Assay for Cellular Growth and Survival: Application to Proliferation and Cytotoxicity Assays,” Journal of Immunological Methods, Vol. 65, No. 1-2, December 1983, pp. 55-63. doi:10.1016/0022-1759(83)90303-4
[24] Y. R. Lea-Currie, et al., “Dehydroepiandrosterone Reduces Proliferation and Differentiation of 3T3-L1 Preadipocytes,” Biochemical and Biophysical Research Com- munications, Vol. 248, No. 3, July 1998, pp. 497-504. doi:10.1006/bbrc.1998.8996
[25] D. L. Satory and S. B. Smith, “Conjugated Linoleic Acid Inhibits Proliferation but Stimulates Lipid Filling of Murine 3T3-L1 Preadipocytes,” Journal of Nutrition, Vol. 129, No. 1, January 1999, pp. 92-97.
[26] A. W. Murray, “Recycling the Cell Cycle: Cyclins Revisited,” Cell, Vol. 116, No. 2, January 2004, pp. 221-234. doi:10.1016/S0092-8674(03)01080-8
[27] C. A. Auld and R. F. Morrison, “Evidence for Cytosolic p27(Kip1) Ubiquitylation and Degradation during Adipocyte Hyperplasia,” Obesity, Vol. 14, No. 12, December 2006, pp. 2136-2144. doi:10.1038/oby.2006.250
[28] D. E. Phelps and Y. Xiong, “Regulation of Cyclin-De- pendent Kinase 4 during Adipogenesis Involves Switching of Cyclin D Subunits and Concurrent Binding of p18INK4c and p27Kip1,” Cell Growth & Differentiation, Vol. 9, No. 8, August 1998, pp. 595-610.
[29] M. A. Ciemerych, et al., “Development of Mice Expressing a Single D-Type Cyclin,” Genes & Development, Vol. 16, No. 24, December 2002, pp. 3277-3289.
[30] M. Hitomi and D. W. Stacey, “Cellular Ras and Cyclin D1 are Required during Different Cell Cycle Periods in Cycling NIH 3T3 Cells,” Molecular and Cellular Biology, Vol. 19, No. 7, July 1999, pp. 4623-4632.
[31] M. De Falco, et al., “Evaluation of Cyclin D1 Expression and Its Subcellular Distribution in Mouse Tissues,” Jour- nal of Anatomy, Vol. 205, No. 5, November 2004, pp. 405-412. doi:10.1111/j.0021-8782.2004.00347.x
[32] D. C. Chung, “Cyclin D1 in Human Neuroendocrine: Tumorigenesis,” Annals of the New York Academy of Sciences, Vol. 1014, 2004, pp. 209-217.
[33] P. Sumrejkanchanakij, et al., “Role of Cyclin D1 Cytop-lasmic Sequestration in the Survival of Postmitotic Neu-rons,” Oncogene, Vol. 22, No. 54, November 2003, pp. 8723-8730. doi:10.1038/sj.onc.1206870
[34] M. C. Liu, J. L. Marshall and R. G. Pestell, “Novel Strategies in Cancer Therapeutics: Targeting Enzymes Involved in Cell Cycle Regulation and Cellular Proliferation,” Current Cancer Drug Targets, Vol. 4, No. 5, August 2004, pp. 403-424. doi:10.2174/1568009043332907
[35] S. Pelengaris and M. Khan, “DNA Replication and the Cell Cycle,” In: S. Pelengaris and M. Khan, Eds., The Molecular Biology of Cancer, Blackwell Publishing Ltd., Oxford, 2006.
[36] R. F. Morrison and S. R. Farmer, “Role of PPARγ in Regulating a Cascade Expression of Cyclin-Dependent Kinase Inhibitors, p18(INK4c) and p21(Waf1/Cip1), during Adipogenesis,” Journal of Biological Chemistry, Vol. 274, No. 24, June 1999, pp. 17088-17097. doi:10.1074/jbc.274.24.17088
[37] W.-C. Chiang, et al., “YC-1-Inhibited Proliferation of Rat Mesangial Cells through Suppression of Cyclin D1—In- dependent of cGMP Pathway and Partially Reversed by p38 MAPK Inhibitor,” European Journal of Pharmacol-ogy, Vol. 517, No. 1-2, July 2005, pp. 1-10. doi:10.1016/j.ejphar.2005.04.046

  
comments powered by Disqus

Copyright © 2018 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.