Effect of Phosphatidylcholine on Dyslipidemia and Atherogenic Index in High Fructose Exposed Rats
Article Sidebar
Main Article Content
Abstract
The purpose of this research was to investigate the beneficial effects of phosphatidylcholine in reducing changes in both lipid and protein profiles in addition to atherogenic index in adult rats with fructose-induced metabolic syndrome. Thirty-six mature Wistar Albino female rats (Rattus norvegicus) (aged 12-15 weeks and weighing 200±10 g) were divided randomly into four groups (G1, G2, G3, and G4); then variable treatments were orally administered for 62 days as follows: G1 (Control group), received distilled water; G2, treated with phosphatidylcholine (PC) orally (1 g/kg BW); G3 (Fr), orally dosed with 40% fructose and 25% fructose mixed with drinking water; G4 (Fr+PC), were also intubated with 40% fructose and 25% fructose in drinking water, and received PC at 1 g/kg BW by oral tube. At the end of the research, specimens were taken by cardio puncture approach after fasting for 8-12 h. Serum was obtained to measure lipid criteria (total serum cholesterol, triacylglycerol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, non-high-density lipoprotein-cholesterol, and Atherogenic index) and protein profile (total protein, albumin, and globulins). The results showed that the occurrence of dyslipidaemia (hypercholesterolemia, triacyleglycerolemia) increase in low density of lipoprotein-cholesterol, very low-density lipoprotein-cholesterol, no-high density lipoprotein-cholesterol concentrations and atherogenic index and reduce the concentration of high-density lipoprotein-cholesterol) in fructose treated animals in addition to disturbance in protein profile (lowered in total protein and globulins level).PC treatment resulted in decreased changes in lipid profile, protein profile, and atherogenic index in rats, whereas fructose induced metabolic syndrome. In conclusion, using Phosphatidylcholine treatment in rats may reduce the changes of lipid and protein profiles and atherogenic index while fructose may lead to metabolic syndrome.
Downloads
Article Details
How to Cite
References
Mirtschink P, Jang C, Arany Z, Krek W. Fructose metabolism cardiometabolic risk and the epidemic of coronary artery disease. Eur. Heart J. 2018; 39(26): 2497– 2505. https://doi.org/10.1093/eurheartj/ehx518
Castro MC, Villagarcía HG, Massa ML, Francini F. Alphalipoic acid and its protective role in fructose induced endocrine-metabolic disturbances. Food & Func. 2019; 10(1):16-25. https://doi.org/10.1039/C8FO01856A
Sartorelli DS, Franco LJ, Gimeno SG, Ferreira SR, Cardoso MA. Dietary fructose, fruits, fruit juices and glucose tolerance status in Japanese Brazilians. Nutr. Metab. Cardiovasc. Dis. 2009; 19(2):77-83. https://doi.org/10.1016/j.numecd.2008.04.004
Ferrier DR. Lippincott’s Illustrated Review: Biochemistry. Seventh Edition. Wolters Kluwer. Lippincott’s William and Wilkins, Health. Philadelphia. Baltimore. 2017; New York. London. Buenos Aires. Hong Kong. Sydney. Tokyo.
Lustig RH, Mulligan K, Noworolski SM, Tai VW, Wen MJ, Erkin- Cakmak A, et al. Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome, Obesity, 2016; 24(2): 453–460. https://doi.org/10.1002/oby.21371
Sreeja S, Geetha R, Priyadarshini E, Bhavani K, Anuradha CV. Substitution of soy protein for casein prevents oxidative modification and inflammatory response induced in rats fed high fructose diet. ISRN inflammation. 2014; 641096. https://doi.org/10.1155/2014/641096
Al-Agele FAL, Khudair KK. Effect of acrylamide and fructose on some parameters related to metabolic syndrome in adult male rats. Iraqi J. Vet. Med., 2016; 40(1): 125–135. https://doi.org/10.30539/iraqijvm.v40i1.149
8. Castro MC, Francini F, Schinella G, Caldiz CI, Zubiría MG, Gagliardino JJ, et al. Apocynin administration prevents the changes induced by a fructose-rich diet on rat liver metabolism and the antioxidant system. Clin. Sci. 2012; (123): 681–692. https://doi.org/10.1042/CS20110665
Caliceti C, Calabria D, Roda A, Cicero AFG. Fructose intake, serum uric acid and cardiometabolic disorders: a critical review. Nutr. 2017; 9: E395. https://doi.org/10.3390/nu9040395
Yin M, Matsuoka R, Xi Y, Wang X. Comparison of Egg Yolk and Soybean phospholipids on Hepatic Fatty Acid Profile and Liver Protection in Rats Fed a High-Fructose Diet. Foods, 2021; 10: 1569. https://doi.org/10.3390/foods10071569
Jang C, Hui S, Lu W, Tesz GJ, Birnbaum MJ, Rabinowitz JD. The small intestine converts dietary fructose into glucose and organic acids. Cell Metab., 2018; 27:351–361. https://doi.org/10.1016/j.cmet.2017.12.016
Hasan BF, Salman IN, AL-Temimi AFH. Metabolic Disturbances of Phosphate in Metabolic Syndrome. Baghdad Sci J. 2014; 11(2): 387-392. https://doi.org/10.21123/bsj.2014.11.2.387-392
Cydylo MA, Davis AT, Kavanagh K. Fatty liver promotes fibrosis in monkeys consuming high fructose. Obesity, Silver Spring. 2017; 25(2): 290–293. https://doi.org/10.1002/oby.21720
Bawden SJ, Stephenson MC, Ciampi E, Hunter K, Marciani L, Macdonald IA, et al. Investigating the effects of an oral fructose challenge on hepatic ATP reserves in healthy volunteers: A (31)P MRS study. Clinical Nutr. 2016; 35(3): 645-649. https://doi.org/10.1016/j.clnu.2015.04.001
Al-rubaye ZS, Al-Shahwany AW. Estimation of Vitamin C and the Fructose Levels in Some Medicinal Plants and their Effects on Iron Bioavailability in Rats. Ira. J. of Sci., 2022; 63(1): 77–86. https://doi.org/10.24996/ijs.2022.63.1.9
Schwarz JM, Noworolski SM, Erkin-Cakmak A, Korn NJ, Wen MJ, Tai VW, et al. Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children with Obesity, Gastroenterology, 2017; 153(3): 743–752. https://doi.org/10.1053/j.gastro.2017.05.043
Johnson R, Sanchez-Lozada L, Andrews P, Lanaspa M. A historical and scientific perspective of sugar and its relation with obesity and diabetes. Adv. Nutr. An. Int. Rev. J. 2017; 8(3): 412-422. https://doi.org/10.3945/an.116.014654
Legeza B, Marcolongo P, Gamberucci A, Varga V, Bánhegyi G, Benedetti A, et al. Fructose, glucocorticoids and adipose tissue: Implications for the metabolic syndrome. Nutrients. 2017; 9(5): 426. https://doi.org/10.3390/nu9050426
Sellmann C, Priebs J, Landmann M, Degen C, Engstler AJ, Jin CJ, et al. Diets rich in fructose, fat or fructose and fat alter intestinal barrier function and lead to the development of nonalcoholic fatty liver disease over time. J. Nutr. Biochem. 2015; 26: 1183–1192. https://doi.org/10.1016/j.jnutbio.2015.05.011
Spruss A, Kanuri G, Wagnerberger S, Haub S, Bischoff SC, Bergheim I. Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice. Hepatol. 2009; 50(4): 1094–1104. https://doi.org/10.1002/hep.23122
Di Luccia B, Crescenzo R, Mazzoli A, Cigliano L, Venditti P, Walser JC, et al. Rescue of fructose-induced metabolic syndrome by antibiotics or faecal transplantation in a rat model of obesity. PLoS ONE, 2015; 10(8): e0134893. https://doi.org/10.1371/journal.pone.0134893
Dogan S, Celikbilek M, Guven K. High fructose consumption can induce endotoxemia. Gastroenterol., 2012; 143(3): e29. https://doi.org/10.1053/j.gastro.2012.07.012
23. Oppelt SA, Zhang W, Tolan DR. Specific regions of the brain are capable of fructose metabolism. Brain Res., 2017; 1657: 312–322. https://doi.org/10.1016/j.brainres.2016.12.022
De Sousa Rodrigues ME, Bekhbat M, Houser MC, Chang J, Walker DI, Jones DP, et al. Chronic psychological stress and high-fat high-fructose diet disrupt metabolic and inflammatory gene networks in the brain, liver, and gut and promote behavioral deficits in mice. Brain Behav. Immun., 2017; 59: 158–172. https://doi.org/10.1016/j.bbi.2016.08.021
Posey KA, Clegg DJ, Printz RL, Byun J, Morton GJ, Vivekanandan-Giri A, et al. Hypothalamic proinflammatory lipid accumulation, inflammation, and insulin resistance in rats fed a high-fat diet. American Journal Physiol. Endo Meta. 2009; 296(5): 1003–1012. https://doi.org/10.1152/ajpendo.90377.2008
Vance JE. Phospholipid synthesis and transport in mammalian cells. Traffic, 2015; 16(1): 1–18. https://doi.org/10.1111/tra.12230
Bashi T, Shovman O, Fridkin M, Volkov A, Barshack I, Blank M, et al. Novel therapeutic compound tuftsin-phosphorylcholine attenuates collagen- induced arthritis. Clin Exp Immunol., 2016; 184: 19-28. https://doi.org/10.1111/cei.12745
Cohn JS, Wat E, Kamili A, Tandy S. Dietary phospholipids, hepatic lipid metabolism and cardiovascular disease. Curr. Opin. Lipidol., 2008; 19: 257–62. https://doi.org/10.1097/MOL.0b013e3282ffaf96
Küllenberg D, Taylor LA, Schneider M, Massing U. Health effects of dietary phospholipids. Lipids Health Dis., 2012; 11:3. https://doi.org/10.1186/1476-511X-11-3
Nicolson GL, Ash ME. Lipid Replacement Therapy: A natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Biochimica et Biophysica Acta (BBA) Biomembranes. 2014; 1838(6):1657–1679. https://doi.org/10.1016/j.bbamem.2013.11.010
Feng L, Liu W, Yang J, Wang Q, Wen S. Effect of Hexadecyl Azelaoyl Phosphatidylcholine on Cardiomyocyte Apoptosis in Myocardial Ischemia-Reperfusion Injury: A Hypothesis. Medical science monitor: Inter. Medical. J. Exp. Clin. Res., 2018; 24: 2661–2667. https://doi.org/10.12659/MSM.907578
Gornall AG, Bardawill CJ, David MM. Determination of serum proteins by means of the biuret reaction. J. Biol. Chem., 1949; 177(2):751-766. USA. https://doi.org/10.1016/S0021-9258(18)57021-6
SAS. Statistical Analysis System, User's Guide. Statistical. Version 9.1 ed. SAS. Inst. Inc. Cary. 2012; N.C.
Haslam DE, McKeown NM, Herman MA, Lichtenstein AH, Dashti HS. “Interactions between genetics and sugar-sweetened beverage consumption on health outcomes: a review of gene–diet interaction studies,” Frontiers in Endocrinol., 2018; 8: 368. https://doi.org/10.3389/fendo.2017.00368
Evans RA, Frese M, Romero J, Cunningham JH, Mills KE. “Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis,” Am. J. Clin. Nutr., 2017; 106(2): 506–518. https://doi.org/10.3945/ajcn.116.145151
Czerwonogrodzka-Senczyna A, Rumińska M, Majcher A, Credo D, Jeznach- Steinhagen A, Pyrżak, B. Fructose Consumption and Lipid Metabolism in Obese Children and Adolescents. In: Pokorski M. (eds) Medical Science and Research. Adv. Exp. Med. Biol., 2019; 1153: 91-100. https://doi.org/10.1007/5584_2018_330
Schwarz MJ, Clearfield M, Mulligan K. Conversion of Sugar to Fat: Is hepatic de novo lipogenesis leading to metabolic syndrome and associated chronic diseases? J. Am. Osteopath. Assoc., 2017; 117: 520-527. https://doi.org/10.7556/jaoa.2017.102
Ramadhan SJ, khudair KK. Effect of Betaine on Hepatic and Renal Functions in Acrylamide Treated Rats. Iraqi J. Vet. Med., 2019; 43(1): 138–147. https://doi.org/10.30539/iraqijvm.v43i1.484
Mortera RR, Bains Y, Gugliucci A. Fructose at the crossroads of the metabolic syndrome and obesity epidemics. Frontiers In Bioscience, Landmark, 2019; 24: 186-211. https://doi.org/10.2741/4713
Song A, Astbury S, Hoedl A, Nielsen B, Symonds ME, Bell RC. Lifetime exposure to a constant environment amplifies the impact of a fructose rich diet on glucose homeostasis during pregnancy. Nutrients. 2017; 9(4). https://doi.org/10.3390/nu9040327
Jung TW, Kim ST, Lee JH, Chae SI, Hwang KW, Chung YH, et al. Phosphatidylcholine Causes lipolysis and apoptosis in adipocytes through the tumor necrosis factor alpha-dependent pathway. Pharmacol. 2018; 101(3-4): 111-119. https://doi.org/10.1159/000481571
Jung TW, Park T, Park J, Kim U, Je HD, et al. Phosphatidylcholine causes adipocyte-specific lipolysis and apoptosis in adipose and muscle tissues. PLOS ONE, 2019; 14(4): e0214760. https://doi.org/10.1371/journal.pone.0214760
Mourad AM, Pincinato EdC, Mazzola PG, Sabha M, Moriel P. Influence of soy lecithin administration on hypercholesterolemia. Cholesterol, 2010: 824813, 4. https://doi.org/10.1155/2010/824813
Hasanain M, Bhattacharjee A, Pandey P, Ashraf R, Singh N, Sharma S, et al. A-solanine induces ROS- mediated autophagy through activation of endoplasmic reticulum stress and inhibition of akt/mtor pathway. Cell Death Dis., 2015; 6: e1860. https://doi.org/10.1038/cddis.2015.219
Plaisance V, Brajkovic S, Tenenbaum M, Favre D, Ezanno H, Bonnefond A, et al. Endoplasmic reticulum stress links oxidative stress to impaired pancreatic β-cell function caused by human oxidized ldl. PLoS ONE 2016; 11: e0163046. https://doi.org/10.1371/journal.pone.0163046
Malhotra JD, Miao H, Zhang K, Wolfson A, Pennathur S, Pipe SW, et al. Antioxidants reduce endoplasmic reticulum stress and improve protein secretion. Proc. Natl. Acad. Sci., 2008; 105: 18525–18530. https://doi.org/10.1073/pnas.0809677105
Balakumar M, Raji L, Prabhu D, Sathishkumar C, Prabu P, Mohan V, Balasubramanyam M. High-fructose diet is as detrimental as high-fat diet in the induction of insulin resistance and diabetes mediated by hepatic/pancreatic endoplasmic reticulum (ER) stress. Mol. Cell. Biochem., 2016; 423(1-2): 93–104. https://doi.org/10.1007/s11010-016-2828-5
Adibhatla RM, Hatcher J.F. Lipid oxidation and peroxidation in CNS health and disease: from molecular mechanisms to therapeutic opportunities. Antioxid Redox Signal, 2010; 12(1):125- 169. https://doi.org/10.1089/ars.2009.2668
Unger RH. Longevity, lipotoxicity and leptin: the adipocyte defense against feasting and famine. Biochimie., 2005; 87(1): 57–64. https://doi.org/10.1016/j.biochi.2004.11.014
Chong WC, Shastri MD, Eri R. Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Nexus Implicated in Bowel Disease Pathophysiology. Int. J. Mol. Sci., 2017; 18(4):771. https://doi.org/10.3390/ijms18040771
Marchio P, Guerra-Ojeda S, Vila JM, Aldasoro M, Victor VM, Mauricio MD. Targeting Early Atherosclerosis: A Focus on Oxidative Stress and Inflammation. Oxidative Medicine and Cellular Longevity. 2019; Article ID 8563845, 32 pages . https://doi.org/10.1155/2019/8563845
Hsia SH, Pan D, Berookim P, Lee ML. A population-based, cross-sectional comparison of lipid-related indexes for symptoms of atherosclerotic disease. Am. J. Cardiol., 2006; 98(8):1047-1052. https://doi.org/10.1016/j.amjcard.2006.05.024
Kim JY, Kwon MS, Son J, Kang SW, Song Y. Selective effect of phosphatidylcholine on the lysis of adipocytes. PLoS ONE, 2017; 12(5): e0176722. https://doi.org/10.1371/journal.pone.0176722
Burgess JW, Neville TA, Rouillard P, Harder, Z, Beanlands DS, Sparks DL. Phosphatidylinositol increases HDL-C levels in humans. J. Lipid Res., 2005; 46(2):350–355. https://doi.org/10.1194/jlr.M400438-JLR200
Cohn JS, Wat E, Kamili A, Tandy S. Dietary phospholipids, hepatic lipid metabolism and cardiovascular disease. Curr. Opin. Lipidol., 2008; 19:257–62. https://doi.org/10.1097/MOL.0b013e3282ffaf96
Nicolosi RJ, Wilson TA, Lawton C, Handelman, GJ. “Dietary effects on cardiovascular disease risk factors: beyond saturated fatty acids and cholesterol. J American College Nutr. 2001; 20(5): 421S–427S. https://doi.org/10.1080/07315724.2001.10719179
Dawod SMH. The effect of soybean lecithin on lipid profile, glycemic index and insulin resistance in hypercholestromic adult male rats. MSc. Thesis/ college of veterinary medicine/ University of Baghdad. 2018.
Diaf M, Khaled MB. Associations between dietary antioxidant intake and markers of atherosclerosis in middle-aged women from North-Western Algeria. Front. Nutr.2018; 5(29). https://doi.org/10.3389/fnut.2018.00029
Lee HS, Yunsung N, Chung YH, Kim HR, Park ES, Chung SJ, Kim JH, Sohn UD, Kim HC, Oh KW, Jeong JH. Beneficial effects of phosphatidylcholine on high-fat diet-induced obesity, hyperlipidemia and fatty liver in mice. Life Sci. 2014; 118(1): 7-14. https://doi.org/10.1016/j.lfs.2014.09.027
Oršolić N, Landeka Jurčević I, Đikić D, Rogić D, Odeh D, Balta V, Perak Junaković E, Terzić S, Jutrić D. ‘Effect of Propolis on Diet-Induced Hyperlipidemia and Atherogenic Indices in Mice’, Antioxidants, 2019; 8(6): 156. https://doi.org/10.3390/antiox8060156
Avelar TMT, Storch AS, Castro LA, Azevedo GVM, Ferraz L, Lopes PF. Oxidative stress in the pathophysiology of metabolic syndrome: which mechanisms are involved. J. Bras. Patol. Med. Lab., 2015; 51(4): 231-239. https://doi.org/10.5935/1676-2444.20150039
Nicolson GL, Ash, ME. Lipid Replacement Therapy: A natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Biochimica et Biophysica Acta (BBA) - Biomembranes, 2014; 1838(6), 1657–1679. https://doi.org/10.1016/j.bbamem.2013.11.010
Nicolson GL, Ash ME. Membrane Lipid Replacement for chronic illnesses, aging and cancer using oral glycerolphospholipid formulations with fructooligosaccharides to restore phospholipid function in cellular membranes, organelles, cells and tissues. Biochimica et Biophysica Acta (BBA) - Biomembranes, 2017; 1859(9): 1704–1724. https://doi.org/10.1016/j.bbamem.2017.04.013
Ellithorpe RA, Settineri R, Jacques B, Nicolson GL. Lipid Replacement Therapy functional food with NT Factor for reducing weight, girth, body mass, appetite, cravings for foods and fatigue while improving blood lipid profiles, Funct. Food Health Dis. 2012; 2 (1): 11–24. https://doi.org/10.31989/ffhd.v2i1.102