PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Czasopismo

2019 | 78 | 1 |

Tytuł artykułu

The differential effects of high-fat and high- -fructose diets on the liver of male albino rat and the proposed underlying mechanisms

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Background: The Western-style diet is characterised by the high intake of energy- -dense foods. Consumption of either high-fructose diet or saturated fat resulted in the development of metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Many researchers studied the effect of high-fat diet (HFD), high-fructose diet (HFruD) and high-fructose high-fat diet (HFHF) on the liver. The missing data are the comparison effect of these groups i.e. are effects of the HFHF diet on the liver more pronounced? So, this study was designed to compare the metabolic and histopathological effect of the HFD, HFruD, and HFHF on the liver. The proposed underlying mechanisms involved in these changes were also studied. Materials and methods: Twenty four rats were divided into four groups: control, HFD, HFruD, and HFHF. Food was offered for 6 weeks. Biochemical, light microscopic, immunohistochemical (Inducible nitric oxide synthase [iNOS] and alpha-smooth muscle actin [α-SMA]), real-time polymerase chain reaction (gene expression of TNF-α, interleukin-6, Bax, BCL-2, and caspase 3), histomorphometric analysis and oxidative/antioxidative markers (thiobarbituric acid reactive substances [TBARS], malondialdehyde [MDA]/glutathione [GSH] and superoxide dismutase [SOD]) were done. Results: The HFD, HFruD and HFHF groups developed a cluster of liver disorders; steatosis, necrosis, inflammation, apoptosis, ballooning degeneration and cytoplasmic vacuolations. Internal metabolic impairments include elevated serum levels of glucose, triglycerides, low density lipoprotein and decreased serum levels of high density lipoprotein and albumin. The immunoreaction of the α-SMA and iNOS was strong in these groups. The oxidant markers (MDA and TBARS) were elevated, while the antioxidant markers (SOD and GSH) were decreased. The area per cent of collagen, inflammatory markers, caspase 3 and Bax were elevated, while the BCL-2/Bax ratio was decreased. The decrease in PAS, antioxidant markers and the elevation of the α-SMA, iNOS, inflammatory and oxidant markers were obvious in the HFHF when compared to that of the other groups. Conclusions: High-fat diet, HFruD, and HFHF developed morphologic hepatic changes ranging from steatosis to necrosis and inflammation, besides the development of internal metabolic impairments. The chief factors of hepatic injury were fat accumulation in the hepatocytes, oxidative stress and highly elevated iNOS. Compared to the other groups, HFHF’s effect was more prominent. (Folia Morphol 2019; 78, 1: 124–136)

Słowa kluczowe

Wydawca

-

Czasopismo

Rocznik

Tom

78

Numer

1

Opis fizyczny

p.124-136,fig.,ref.

Twórcy

autor
  • Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt
  • Fakeeh College for Medical Sciences, Jeddah, Saudi Arabia
autor
  • Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt
autor
  • Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Cairo, Egypt

Bibliografia

  • 1. Adams JM, Cory S. The Bcl-2 protein family: arbiters of cell survival. Science. 1998; 281(5381): 1322–1326, indexed in Pubmed: 9735050.
  • 2. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009; 120(16): 1640–1645, doi: 10.1161/CIRCULATIONAHA.109.192644, indexed in Pubmed: 19805654.
  • 3. Angulo P, Lindor KD. Non-alcoholic fatty liver disease. J Gastroenterol Hepatol. 2002; 17(Suppl): S186–S190.
  • 4. Asakawa T, Yagi M, Tanaka Y, et al. The herbal medicine Inchinko-to reduces hepatic fibrosis in cholestatic rats. Pediatr Surg Int. 2012; 28(4): 379–384, doi: 10.1007/s00383-011-2974-5, indexed in Pubmed: 22045203.
  • 5. Birben E, Sahiner U, Sackesen C, et al. Oxidative stress and antioxidant defense. World Allergy Organization J. 2012; 5(1): 9–19, doi: 10.1097/wox.0b013e3182439613.
  • 6. Bocarsly ME, Powell ES, Avena NM, et al. High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacol Biochem Behav. 2010; 97(1): 101–106, doi: 10.1016/j.pbb.2010.02.012, indexed in Pubmed: 20219526.
  • 7. Browning JD, Horton JD. Molecular mediators of hepatic steatosis and liver injury. J Clin Invest. 2004; 114(2): 147–152, doi: 10.1172/JCI22422, indexed in Pubmed: 15254578.
  • 8. Collins S, Martin TL, Surwit RS, et al. Genetic vulnerability to diet-induced obesity in the C57BL/6J mouse: physiological and molecular characteristics. Physiol Behav. 2004; 81(2): 243–248, doi: 10.1016/j.physbeh.2004.02.006, indexed in Pubmed: 15159170.
  • 9. Collison KS, Zaidi MZ, Saleh SM, et al. Effect of trans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile. Br J Nutr. 2011; 106(2): 218–226, doi: 10.1017/S000711451000588X, indexed in Pubmed: 21429276.
  • 10. Costa E, Rezende B, Cortes S, et al. Neuronal Nitric Oxide Synthase in Vascular Physiology and Diseases. Front Physiol. 2016; 7, doi: 10.3389/fphys.2016.00206.
  • 11. Day CP, James OF. Hepatic steatosis: innocent bystander or guilty party? Hepatology. 1998; 27(6): 1463–1466, doi: 10.1002/hep.510270601, indexed in Pubmed: 9620314.
  • 12. Day CP, James OF. Steatohepatitis: a tale of two “hits”? Gastroenterology. 1998; 114(4): 842–845, indexed in Pubmed: 9547102.
  • 13. Dröge W. Free radicals in the physiological control of cell function. Physiol Rev. 2002; 82(1): 47–95, doi: 10.1152/physrev.00018.2001, indexed in Pubmed: 11773609.
  • 14. Feldstein A, Gores G. Steatohepatitis and apoptosis: therapeutic implications. Am J Gastroenterol. 2004; 99(9): 1718–1719, doi: 10.1111/j.1572-0241.2004.40573.x.
  • 15. Feldstein A, Canbay A, Angulo P, et al. Hepatocyte apoptosis and fas expression are prominent features of human nonalcoholic steatohepatitis. Gastroenterology. 2003; 125(2): 437–443, doi: 10.1016/s0016-5085(03)00907-7.
  • 16. Folch J, Lees M, Sloane Stanley GH. A simple method for the isolation and purification of total lipides from animal tissues. J Biol Chem. 1957; 26(1): 497–509.
  • 17. Ha SK, Chae C. Inducible nitric oxide distribution in the fatty liver of a mouse with high fat diet-induced obesity. Exp Anim. 2010; 59(5): 595–604, indexed in Pubmed: 21030787.
  • 18. Hebbard L, George J. Animal models of nonalcoholic fatty liver disease. Nat Rev Gastroenterol Hepatol. 2011; 8(1): 35–44, doi: 10.1038/nrgastro.2010.191, indexed in Pubmed: 21119613.
  • 19. Jurdak N, Lichtenstein AH, Kanarek RB. Diet-induced obesity and spatial cognition in young male rats. Nutr Neurosci. 2008; 11(2): 48–54, doi: 10.1179/147683008X301333, indexed in Pubmed: 18510803.
  • 20. Larter CZ, Yeh MM. Animal models of NASH: getting both pathology and metabolic context right. J Gastroenterol Hepatol. 2008; 23(11): 1635–1648, doi: 10.1111/j.1440-1746.2008.05543.x, indexed in Pubmed: 18752564.
  • 21. Lee JS, Jun DW, Kim EK, et al. Histologic and metabolic derangement in high-fat, high-fructose, and combination diet animal models. ScientificWorldJournal. 2015; 2015: 306326, doi: 10.1155/2015/306326, indexed in Pubmed: 26090514.
  • 22. Li S, Liao X, Meng F, et al. Therapeutic role of ursolic acid on ameliorating hepatic steatosis and improving metabolic disorders in high-fat diet-induced non-alcoholic fatty liver disease rats. PLoS One. 2014; 9(1): e86724, doi: 10.1371/journal.pone.0086724, indexed in Pubmed: 24489777.
  • 23. Ma J, Zou C, Guo L, et al. Novel Death Defying Domain in Met entraps the active site of caspase-3 and blocks apoptosis in hepatocytes. Hepatology. 2014; 59(5): 2010–2021, doi: 10.1002/hep.26769, indexed in Pubmed: 24122846.
  • 24. Miele L, Valenza V, La Torre G, et al. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Hepatology. 2009; 49(6): 1877–1887, doi: 10.1002/hep.22848, indexed in Pubmed: 19291785.
  • 25. Pereira-Lancha LO, Campos-Ferraz PL, Lancha AH. Obesity: considerations about etiology, metabolism, and the use of experimental models. Diabetes Metab Syndr Obes. 2012; 5: 75–87, doi: 10.2147/DMSO.S25026, indexed in Pubmed: 22570558.
  • 26. Peverill W, Powell LW, Skoien R. Evolving concepts in the pathogenesis of NASH: beyond steatosis and inflammation. Int J Mol Sci. 2014; 15(5): 8591–8638, doi: 10.3390/ijms15058591, indexed in Pubmed: 24830559.
  • 27. Ribeiro PS, Cortez-Pinto H, Solá S, et al. Hepatocyte apoptosis, expression of death receptors, and activation of NF-kappaB in the liver of nonalcoholic and alcoholic steatohepatitis patients. Am J Gastroenterol. 2004; 99(9): 1708–1717, doi: 10.1111/j.1572-0241.2004.40009.x, indexed in Pubmed: 15330907.
  • 28. Rolo AP, Teodoro JS, Palmeira CM. Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis. Free Radic Biol Med. 2012; 52(1): 59–69, doi: 10.1016/j.freeradbiomed.2011.10.003, indexed in Pubmed: 22064361.
  • 29. Schwartz DM, Wolins NE. A simple and rapid method to assay triacylglycerol in cells and tissues. J Lipid Res. 2007; 48(11): 2514–2520, doi: 10.1194/jlr.D700017-JLR200, indexed in Pubmed: 17717377.
  • 30. Sheehan DC, Hrapchak BB. Theory and practice of histotechnology. 2d edn. Mosby, St Louis 1980.
  • 31. Spruss A, Kanuri G, Wagnerberger S, et al. Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice. Hepatology. 2009; 50(4): 1094–1104, doi: 10.1002/hep.23122, indexed in Pubmed: 19637282.
  • 32. Stark AH, Timar B, Madar Z. Adaptation of Sprague Dawley rats to long-term feeding of high fat or high fructose diets. Eur J Nutr. 2000; 39(5): 229–234, indexed in Pubmed: 11131370.
  • 33. Takaki A, Kawai D, Yamamoto K. Multiple hits, including oxidative stress, as pathogenesis and treatment target in non-alcoholic steatohepatitis (NASH). Int J Mol Sci. 2013; 14(10): 20704–20728, doi: 10.3390/ijms141020704, indexed in Pubmed: 24132155.
  • 34. Teli MR, James OF, Burt AD, et al. The natural history of nonalcoholic fatty liver: a follow-up study. Hepatology. 1995; 22(6): 1714–1719, indexed in Pubmed: 7489979.
  • 35. Thornberry NA, Lazebnik Y. Caspases: enemies within. Science. 1998; 281(5381): 1312–1316, indexed in Pubmed: 9721091.
  • 36. Tipple TE, Rogers LK. Methods for the determination of plasma or tissue glutathione levels. Methods Mol Biol. 2012; 889: 315–324, doi: 10.1007/978-1-61779-867-2_20, indexed in Pubmed: 22669674.
  • 37. Tsujimoto Y. Role of Bcl-2 family proteins in apoptosis: apoptosomes or mitochondria? Genes to Cells. 1998; 3(11): 697–707, doi: 10.1046/j.1365-2443.1998.00223.x.
  • 38. Wang MY, Grayburn P, Chen S, et al. Adipogenic capacity and the susceptibility to type 2 diabetes and metabolic syndrome. Proc Natl Acad Sci U S A. 2008; 105(16): 6139–6144, doi: 10.1073/pnas.0801981105, indexed in Pubmed: 18413598.
  • 39. Wang Y, Ausman LM, Russell RM, et al. Increased apoptosis in high-fat diet-induced nonalcoholic steatohepatitis in rats is associated with c-Jun NH2-terminal kinase activation and elevated proapoptotic Bax. J Nutr. 2008; 138(10): 1866–1871, doi: 10.1093/jn/138.10.1866, indexed in Pubmed: 18806094.
  • 40. Weydert CJ, Cullen JJ. Measurement of superoxide dismutase, catalase and glutathione peroxidase in cultured cells and tissue. Nat Protoc. 2010; 5(1): 51–66, doi: 10.1038/nprot.2009.197, indexed in Pubmed: 20057381.
  • 41. Woodie L, Blythe S. The differential effects of high-fat and high-fructose diets on physiology and behavior in male rats. Nutr Neurosci. 2018; 21(5): 328–336, doi: 10.1080/1028415X.2017.1287834, indexed in Pubmed: 28195006.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

bwmeta1.element.agro-4f501080-ca0e-40c7-9dc0-d9a16d22b24b
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.