Commenced in January 2007
Frequency: Monthly
Edition: International
Paper Count: 33093
Effects of Boron Compounds in Rabbits Fed High Protein and Energy Diet: A Metabolomic and Transcriptomic Approach
Authors: N. Baspinar, A. Basoglu, O. Ozdemir, C. Ozel, F. Terzi, O. Yaman
Abstract:
Current research is targeting new molecular mechanisms that underlie non-alcoholic fatty liver disease (NAFLD) and associated metabolic disorders like non-alcoholic steatohepatitis (NASH). Forty New Zealand White rabbits have been used and fed a high protein (HP) and energy diet based on grains and containing 11.76 MJ/kg. Boron added to 3 experimental groups’ drinking waters (30 mg boron/L) as boron compounds. Biochemical analysis including boron levels, and nuclear magnetic resonance (NMR) based metabolomics evaluation, and mRNA expression of peroxisome proliferator-activated receptor (PPAR) family was performed. LDLcholesterol concentrations alone were decreased in all the experimental groups. Boron levels in serum and feces were increased. Content of acetate was in about 2x higher for anhydrous borax group, at least 3x higher for boric acid group. PPARα mRNA expression was significantly decreased in boric acid group. Anhydrous borax attenuated mRNA levels of PPARγ, which was further suppressed by boric acid. Boron supplementation decreased the degenerative alterations in hepatocytes. Except borax group other boron groups did not have a pronounced change in tubular epithels of kidney. In conclusion, high protein and energy diet leads hepatocytes’ degenerative changes which can be prevented by boron supplementation. Boric acid seems to be more effective in this situation.Keywords: High protein and energy diet, boron, metabolomic, transcriptomic.
Digital Object Identifier (DOI): doi.org/10.5281/zenodo.1107147
Procedia APA BibTeX Chicago EndNote Harvard JSON MLA RIS XML ISO 690 PDF Downloads 1995References:
[1] N. Sattar, E Forrest, and D. Preiss, “Non-alcoholic fatty liver disease,” BMJ, vol. 29, no: 349, g4596, 2014.
[2] J. K. Dyson, Q. M. Anstee, and S. McPherson, “Non-alcoholic fatty liver disease: a practical approach to treatment,” Frontline Gastroenterol., vol. 5, pp. 277-286, 2014.
[3] M. Diez, and P. Nguyen, “The epidemiology of canine and feline obesity,” Focus, vol. 16, pp. 2-8, 2006.
[4] S. C. Garcia-Caraballo, T. M. Comhair, F. Verheyen, I. Gaemers, F. G. Schaap, S. M. Houten, T. B. Hakvoort, C. H. Dejong, W. H. Lamers, and S. H. Koehler, “Prevention and reversal of hepatic steatosis with a high-protein diet in mice,” Biochim.Biophys. Acta., vol. 1832, pp. 685-695, 2013.
[5] K. Yasutake, M. Kohjima, K. Nakashima, M. Kotoh, M. M. Nakamuta, and M. Enjoji, “Nutrition therapy for liver diseases based on the status of nutritional intake,” Gastroenterol. Res. Pract., vol. 2012, 859697, 2012.
[6] J. G. Fan, and H. X. Cao, “Role of diet and nutritional management in non-alcoholic fatty liver disease,”. J. Gastroenterol. Hepatol., vol. 28 Suppl 4, pp. 81-87, 2013.
[7] J. Schwarz, D. Tomé, A. Baars, G. J. Hooiveld, and M. Müller, “Dietary protein affects gene expression and prevents lipid accumulation in the liver in mice,” PLoS One, vol. 7, e47303, 2012.
[8] Y. Terashima, S. Nishiumi, A. Minami, Y. Kawano, N. Hoshi, T. Azuma, and M. Yoshida, “Metabolomics-based search for therapeutic agents for non-alcoholic steatohepatitis,” Arch. Biochem. Biophys., vol. 555-56, pp. 55-65, 2014.
[9] J. G. Neels, and P. A. Grimaldi, “Physiological functions of peroxisome proliferator-activated receptor β,” Physiol. Rev., vol. 94, pp. 795-858, 2014.
[10] S. S. Choi, J. Park, and J. H. Choi, “PPARγ as a revisiting target for treatment of metabolic disorders,” BMB Rep., vol. 25. pii: 2934, 2014.
[11] S. Rauschert, O. Uhl, B. Koletzko, and C. Hellmuth, “Metabolomic biomarkers for obesity in humans: a short review,” Ann. Nutr. Metab., vol. 64: 314-24, 2014.
[12] F. H. Nielsen, “Update on human health effects of boron,” J. Trace Elem. Med. Biol., vol. 28: 383-387, 2014.
[13] A. Basoglu, N. Baspinar, S. A. Ozturk, and P. P. Akalin, “Effects of boron administration on hepatic steatosis, hematological and biochemical profiles in obese rabbits,” Trace Elements and Electrolytes, vol. 27, pp. 225-231, 2010.
[14] A. Basoglu, N. Baspinar, S. A. Ozturk, and P. P. Akalin,“Effects of long-term boron administrations on high-energy diet-induced obesity in rabbits: NMR-based metabonomic evaluation,” J. Anim. Vet. Adv., vol. 10: 1512-1515, 2011.
[15] E. Kurar, M. O. Atli, A. Guzeloglu, Y. Ozsensoy, A. Semacan, “Comparison of five different RNA isolation methods from equine endometrium for gene transcription analysis,” Kafkas Univ. Vet. Fak. Derg., vol. 16, pp. 851–855, 2010.
[16] C. Zou, H. Qi, Z. Liu, L. Han, C. Zhao, and X. Yang, “Simvastatin activates the PPARγ-dependent pathway to prevent left ventricular hypertrophy associated with inhibition of Rhoa signaling,” Tex. Heart Inst. J., vol. 40, pp. 140–147, 2013.
[17] K. J. Livak, and T. D. Schmittgen, “Analysis of relative gene expression data using real-time quantitative PCR and the 2 (-Delta Delta C(T)) Method,” Methods, vol. 25, pp. 402-408, 2001.
[18] H. G. Shertzer, S. E. Woods, M. Krishan, M. B. Genter, and K.J. Pearson, “Dietary whey protein lowers the risk for metabolic disease in mice fed a high-fat diet,” Nutr., vol. 141, pp. 582–587, 2001.
[19] M. Lacroix, C. Gaudichon, A. Martin, C. Morens, V. Mathe, D. Tomé, and J.F. Huneau, “A long term high-protein diet markedly reduces adipose tissue without major side effects in Wistar male rats,” Am. J. Physiol. Regul. Integr. Comp. Physiol., vol. 287, R934–942, 2004.
[20] G. Wu, “Amino acids: metabolism, functions, and nutrition,” Amino Acids, vol. 37, pp. 1–17, 2009.
[21] J. M. Ordovás Muñoz, “Predictors of obesity: the "power" of the omics,” Nutr. Hosp., 28 Suppl, vol. 5, pp. 63-71, 2013.
[22] D. Beyoglu, and J. R. Idle, “The metabolomic window into hepatobiliary disease,” J. Hepatol., vol. 59, pp. 842-858, 2013.
[23] D. Beyoglu, J. R. Idle, “Metabolomics and its potential in drug development,” Biochem. Pharmacol., vol. 85, pp, 12–20, 2013.
[24] H. Li, L. Wang, X. Yan, Q. Liu, C. Yu, H. Wei,Y. Li,X. Zhang, F. He, and Y. Jiang, “A proton nuclear magnetic resonance metabonomics approach for biomarker discovery in nonalcoholic fatty liver disease,” J. Proteome Res., vol. 10,. 2797–2806, 2011.
[25] Z. Ament, M. Masoodi, and J. L. Griffin, “Applications of metabolomics for understanding the action of peroxisome proliferator-activated receptors (PPARs) in diabetes, obesity and cancer,” Genome Med.,vol. 30, no. 4, pp. 32, 2012.
[26] V. G. Giby, and T. A. Ajith, “Role of a dipokines and peroxisome proliferator-activated receptors in nonalcoholic fatty liver disease,” World J. Hepatol., vol. 27, pp. 570-579, 2014.