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Volume 16, Issue 3 (May-Jun 2022)
mljgoums 2022, 16(3): 7-13 |
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Eslami Z, Mohammadnajad Panah kandi Y, Norouzi A, Eghbal Moghanlou A, Sheikh arabi M, Kazeminejad V, et al . Changes in Blood Lipids and Enzymatic Reactions in Response to Atorvastatin Administration Following a High-Fat Diet in a NAFLD Rat Model. mljgoums 2022; 16 (3) :7-13
URL: http://mlj.goums.ac.ir/article-1-1404-en.html
URL: http://mlj.goums.ac.ir/article-1-1404-en.html
Zahra Eslami1 
, Yahya Mohammadnajad Panah kandi2 , Alireza Norouzi3 , Abdorreza Eghbal Moghanlou4 , Mehdi Sheikh arabi5 , Vahideh Kazeminejad6 , Seyedeh somayeh Hosseini alarzi7 , Aref Saeidi8 , Hamidreza Joshaghani 9
, Yahya Mohammadnajad Panah kandi2 , Alireza Norouzi3 , Abdorreza Eghbal Moghanlou4 , Mehdi Sheikh arabi5 , Vahideh Kazeminejad6 , Seyedeh somayeh Hosseini alarzi7 , Aref Saeidi8 , Hamidreza Joshaghani 9
1- Metabolic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Golestan province, Iran
2- Department of Sport PhysiologyIslamic Azad University, Islamshahr Branch, Islamshahr, Iran
3- Golestan Research Center of Gastroenterology and Hepatology, GolestanUniversity of Medical Sciences, Gorgan, Iran
4- farhangian University, Ardebil, Iran
5- Golestan University of Medical Sciences and Health Services, Gorgan, Iran
6- Department of phatology, Golestan University of Medical Sciences and Health Services, Gorgan, Iran
7- Laboratory Science research center, faculty of Paramedicine of Golestan University of medical sciences, Gorgan, Iran
8- Department of Sport Physiotraphy, University of Lahore, Panjab, Pakistan
9- Laboratory Science research center, faculty of Paramedicine of Golestan University of medical sciences, Gorgan, Iran ,hr.joshaghani99@gmail.com
2- Department of Sport PhysiologyIslamic Azad University, Islamshahr Branch, Islamshahr, Iran
3- Golestan Research Center of Gastroenterology and Hepatology, GolestanUniversity of Medical Sciences, Gorgan, Iran
4- farhangian University, Ardebil, Iran
5- Golestan University of Medical Sciences and Health Services, Gorgan, Iran
6- Department of phatology, Golestan University of Medical Sciences and Health Services, Gorgan, Iran
7- Laboratory Science research center, faculty of Paramedicine of Golestan University of medical sciences, Gorgan, Iran
8- Department of Sport Physiotraphy, University of Lahore, Panjab, Pakistan
9- Laboratory Science research center, faculty of Paramedicine of Golestan University of medical sciences, Gorgan, Iran ,
Abstract: (3584 Views)
Background and objectives: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by the accumulation of large amounts of fat in the hepatocytes. Given that atorvastatin is effective for treatment of NAFLD, the present study investigated effects of high-fat/fructose diet (HFFD) with atorvastatin on liver enzymes and lipid profile in a NAFLD rat model.
Methods: Thirty-two male Wistar rats were divided into four groups: 1) normal control, 2) HFFD control, 3) HFFD + atorvastatin, and 4) normal + atorvastatin. The groups received HFFD for 15 weeks to induce hepatosteatosis. Atorvastatin was administrated at the dose of 10 mg/kg/day. Lipid profile and liver enzymes were measured after eight weeks of intervention.
Results: Triglyceride, cholesterol, gamma-glutamyl transferase, and aspartate transaminase were significantly reduced in the HFFD + atorvastatin group compared with the HFFD control group. In addition, cholesterol, high-density lipoprotein, alkaline phosphatase, and gamma-glutamyl transferase were significantly increased in the normal + atorvastatin group compared with the normal control group. Low-density lipoprotein increased significantly in the HFFD + atorvastatin group and the normal + atorvastatin group compared with other groups. There was a significant difference in the alanine transaminase levels between the groups taking atorvastatin. In fact, alanine transaminase level was lowest in the normal + atorvastatin group.
Conclusion: Atorvastatin improves the lipid profile and fatty liver and controls liver enzymes. Therefore, it can be used with caution to improve the lipid profile and reduce the complications of NAFLD.
Methods: Thirty-two male Wistar rats were divided into four groups: 1) normal control, 2) HFFD control, 3) HFFD + atorvastatin, and 4) normal + atorvastatin. The groups received HFFD for 15 weeks to induce hepatosteatosis. Atorvastatin was administrated at the dose of 10 mg/kg/day. Lipid profile and liver enzymes were measured after eight weeks of intervention.
Results: Triglyceride, cholesterol, gamma-glutamyl transferase, and aspartate transaminase were significantly reduced in the HFFD + atorvastatin group compared with the HFFD control group. In addition, cholesterol, high-density lipoprotein, alkaline phosphatase, and gamma-glutamyl transferase were significantly increased in the normal + atorvastatin group compared with the normal control group. Low-density lipoprotein increased significantly in the HFFD + atorvastatin group and the normal + atorvastatin group compared with other groups. There was a significant difference in the alanine transaminase levels between the groups taking atorvastatin. In fact, alanine transaminase level was lowest in the normal + atorvastatin group.
Conclusion: Atorvastatin improves the lipid profile and fatty liver and controls liver enzymes. Therefore, it can be used with caution to improve the lipid profile and reduce the complications of NAFLD.
Research Article: Research Article |
Subject:
Biochemistry
Received: 2021/07/13 | Accepted: 2021/08/7 | Published: 2022/05/14 | ePublished: 2022/05/14
Received: 2021/07/13 | Accepted: 2021/08/7 | Published: 2022/05/14 | ePublished: 2022/05/14
References
1. Johnson NA, Sachinwalla T, Walton DW, Smith K, Armstrong A, Thompson MW, et al. Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss. Hepatology. 2009 ;50(4):1105-12. [View at Publisher] [DOI:10.1002/hep.23129] [PubMed] [Google Scholar]
2. Zelber-Sagi S, Ratziu V, Oren R. Nutrition and physical activity in NAFLD: an overview of the epidemiological evidence. World J Gastroenterol. 2011; 17(29): 3377-89. [DOI:10.3748/wjg.v17.i29.3377] [PubMed] [Google Scholar]
3. Hallsworth K, Fattakhova G, Hollingsworth KG, Thoma C, Moore S, Taylor R, et al. Resistance exercise reduces liver fat and its mediators in non-alcoholic fatty liver disease independent of weight loss. Gut. 2011; 60(9): 1278-83. [DOI:10.1136/gut.2011.242073] [PubMed] [Google Scholar]
4. Tazhibi m, Kelishadi r, KHalili Tahmasebi h, Adibi a, Beihaghi a, Salehi hr, et al. Association of lifestyle with metabolic syndrome and non-alcoholic fatty liver in children and adolescence. Hormozgan medical journal. 2010; 14(2): 115-123. [View at Publisher] [Google Scholar]
5. Seyed Khoei, Nazli; Hosseini, Saeed Meraat, Shahin, Golestan, et al. Evaluation of resting metabolism, body composition and some blood structures in men with non-alcoholic fatty liver and its comparison with healthy men. Iranian Journal of Diabetes and Lipids. 2011; 10 (1): 98-101. [View at Publisher] [Google Scholar]
6. Orangi E, Ostad Rahimi A, Mahdavi R, Somi M H, Tarzemani M K. Oxidative Stress-related Parameters and Antioxidant Status in Non-alcoholic Fatty Liver Disease Patients. Iranian Journal of Endocrinology and Metabolism. 2011; 12(5): 493-499. [View at Publisher] [PubMed] [Google Scholar]
7. Tarantino G, Saldalamacchia G, Conca P, Arena A. Non-alcoholic fatty liver disease: Further expression of the metabolic syndrome. JGH. 2007; 22(3): 293-303. [View at Publisher] [PubMed] [Google Scholar]
8. Qureshi K, Abrams GA. Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease. World J Gastroenterol. 2007 14;13(26):3540-53. [View at Publisher] [DOI:10.3748/wjg.v13.i26.3540] [PubMed] [Google Scholar]
9. Barzegarzadeh-Zarandi H, Dabidy-Roshan V.Changes in some liver enzymes and blood lipid level following interval and continuous regular aerobic training in old rats. J Shahrekord Univ Med Sci. 2012; 14(5): 13-23. [View at Publisher] [Google Scholar]
10. Mulhall BP, Ong JP, younossi zm. Non- alacoholic fatty liver disease: an over view. J GastroentrolHepatol. 2002; 17: 1136-43. [View at Publisher] [DOI:10.1046/j.1440-1746.2002.02881.x] [Google Scholar]
11. Mirdar S, Raisi M, Nobahar M. The effect of two-peak exercise training program on some of hepatic stress indexes in active girls. Metabolism and Exercise. 2011; 1(1):11-23. [View at Publisher] [PubMed] [Google Scholar]
12. Chan DF, Li AM, Chu WC, Chan MH, Wong EM, Liu EK, et al. Hepatic steatosis in obese Chinese children. Int J Obes Relat Metab Disord. 2004; 28(10): 1257-63. [View at Publisher] [DOI:10.1038/sj.ijo.0802734] [PubMed] [Google Scholar]
13. Kubota N, Kado S, Kano M, Masuoka N, Nagata Y, Kobayashi T, et al. A high-fat diet and multiple administration of carbon tetrachloride induces liver injury and pathological features associated with non-alcoholic steatohepatitis in mice. Clin Exp Pharmacol Physiol. 2013; 40(7): 422-30. [View at Publisher] [DOI:10.1111/1440-1681.12102] [PubMed] [Google Scholar]
14. Tsuchida T, Lee YA, Fujiwara N, Ybanez M, Allen B, Martins S, et al. A simple diet- and chemical-induced murine NASH model with rapid progression of steatohepatitis, fibrosis and liver cancer. J Hepatol. 2018; 69(2): 385-95. [View at Publisher] [DOI:10.1016/j.jhep.2018.03.011] [PubMed] [Google Scholar]
15. Zhang G, Wang X, Chung TY, Ye W, Hodge L, Zhang L, et al. Carbon tetrachloride (CCl4) accelerated development of non-alcoholic fatty liver disease (NAFLD)/steatohepatitis (NASH) in MS-NASH mice fed western diet supplemented with fructose (WDF). BMC Gastroenterol. 2020; 15; 20(1): 339. [View at Publisher] [DOI:10.21203/rs.3.rs-30324/v1] [PubMed] [Google Scholar]
16. Ridker PM, Rifai N, Pfeffer MA, Sacks FM, Moye LA, Goldman S, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation. 1998; 98(9): 839-44. [DOI:10.1161/01.CIR.98.9.839] [PubMed] [Google Scholar]
17. Steinberg D. Hypercholesterolemia and inflammation in atherogenesis: two sides of the same coin. Mol Nutr Food Res. 2005; 49(11): 995-8. [View at Publisher] [DOI:10.1002/mnfr.200500081] [PubMed] [Google Scholar]
18. Yan-Wang A, HeChang A, JunZou BC, XinJin B, Zhongquan QI. The effect of atorvastatin on m-RNA levels of inflammatorygenes expressionin human peripheral blood lymphocytes by DNA microarray. Biomed Pharmacother. 2011; 65(2): 118-22. [View at Publisher] [DOI:10.1016/j.biopha.2010.12.005] [Google Scholar]
19. Eslami Z, Mirghani SJ, Moghanlou AE, Norouzi A, Naseh H, Joshaghani H, et al. An Efficient Model of Non-alcoholic Fatty Liver Disease (NAFLD) Versus Current Experimental Models: Effects of Fructose, Fat, and Carbon Tetrachloride on NAFLD. Hepat Mon. 2021;21(8): e117696. [View at Publisher] [DOI:10.5812/hepatmon.117696] [Google Scholar]
20. Ness GC, Chambers CM. Feedback and hormonal regulation of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase: the concept of cholesterol buffering capacity. Proc Soc Exp Biol Med. 2000; 224(1): 8-19. [View at Publisher] [DOI:10.1046/j.1525-1373.2000.22359.x] [PubMed] [Google Scholar]
21. Endo A. The discovery and development of HMG-CoA reductase inhibitors. J Lipid Res. 1992; 33: 1569-82. [View at Publisher] [DOI:10.1016/S0022-2275(20)41379-3] [PubMed] [Google Scholar]
22. Wilcox LJ, Barrett PHR, Huff MW. Differential regulation of apolipoprotein B secretion from HepG2 cells by two HMG-CoA reductase inhibitors, atorvastatin and simvastatin. J Lipid Res. 1999; 40: 1078-89. [View at Publisher] [DOI:10.1016/S0022-2275(20)33512-4] [PubMed] [Google Scholar]
23. Ness GC, Chambers CM, Lopez D. Atorvastatin action involves diminished recovery of hepatic HMG-CoA reductase activity. J. Lipid Res. 1998; 39: 75-84. [View at Publisher] [DOI:10.1016/S0022-2275(20)34205-X] [PubMed] [Google Scholar]
24. Burnett JR, Wilcox LJ, Telford DE, Kleinstiver SJ, Barrett PH, Newton RS, et al.The magnitude of decrease in hepatic very low density lipoprotein apolipoprotein B secretion is determined by the extent of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition in miniature pigs. Endocrinology. 1999; 140(11): 5293-302. [View at Publisher] [DOI:10.1210/endo.140.11.7150] [PubMed] [Google Scholar]
25. Wibaut-Berlaimont V, Randi AM, Mandryko V, Lunnon MW, Haskard DO, Naoumova RP. Atorvastatin affects leukocyte gene expression in dyslipidemia patients: in vivo regulation of hemostasis, inflammation and apoptosis. J Thromb Haemost. 2005; 3(4): 677-85. [View at Publisher] [DOI:10.1111/j.1538-7836.2005.01211.x] [PubMed] [Google Scholar]
26. Gouni-Berthold I, Berthold HK, Gylling H, Hallikainen M, Giannakidou E, Stier S, et al. Effects of ezetimibe and/or simvastatin on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase gene expression: a randomized trial in healthy men. Atherosclerosis. 2008; 198(1): 198-207. [View at Publisher] [DOI:10.1016/j.atherosclerosis.2007.09.034] [PubMed] [Google Scholar]
27. Cuthbert JA, Russell DW, Lipsky PE. Regulation of low densitiy lipoprotein receptor gene expression in human lymphocytes. J Biol Chem. 1989; 264: 1298-304. [DOI:10.1016/S0021-9258(19)85085-8] [Google Scholar]
28. Harwood HJ Jr, Bridge DM, Stacpoole PW. In vivo regulation of human mononuclear leukocyte 3-hydroxy-3-methylglutaryl coenzyme A reductase. Studies in normal subjects. J Clin Invest. 1987; 79(4): 1125-32. [View at Publisher] [DOI:10.1172/JCI112928] [PubMed] [Google Scholar]
29. Boucher P, de Lorgeril M, Salen P, Crozier P, Delaye J, Vallon JJ, et al. Effect of dietary cholesterol on low density lipoprotein-receptor, 3-hydroxy-3-methylglutaryl-CoA reductase, and low density lipoprotein receptor-related protein mRNA expression in healthy humans. Lipids. 1998; 33(12): 1177-86. [View at Publisher] [DOI:10.1007/s11745-998-0321-8] [PubMed] [Google Scholar]
30. Powell EE, Kroon PA. Low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl coenzyme A reductase gene expression in human mononuclear leukocytes is regulated coordinately and parallels gene expression in human liver. J Clin Invest. 1994; 93(5): 2168-74. [View at Publisher] [DOI:10.1172/JCI117213] [PubMed] [Google Scholar]
31. BrownWV. Safety of statins. Curr Opin Lipidol. 2008; 19(6): 558-62. [DOI:10.1097/MOL.0b013e328319baba] [PubMed]
32. Ramkumar S, Raghunath A, Raghunath S. Statin Therapy: Review of Safety and Potential Side Effects. Acta Cardiol Sin. 2016 ;32(6):631-639. [PubMed] [Google Scholar]
33. Karanpour Gibchag Z, Heidari R, Abtshi FroushaniM. The effect of combined atorvastatin and zinc sulfate on serum levels of glucose and lipids in type i diabetic rats. Stud Med Sci. 2017; 28(9): 507-19. [View at Publisher] [Google Scholar]
34. Ebrahimi Daryani N, Hashtroudi AA. Drug induced liver diseases. J Med Couac IR Iran. 2004; 22 (2): 129-50. [View at Publisher] [Google Scholar]
35. Ji G, Zhao X, Leng L, Liu P, Jiang Z. Comparison of dietary control and atorvastatin on high fat diet induced hepatic steatosis and hyperlipidemia in rats. Lipids Health Dis. 2011; 10: 23. [View at Publisher] [DOI:10.1186/1476-511X-10-23] [PubMed] [Google Scholar]
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