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VİTAMİN D EKSİKLİĞİ SIÇANLARDA ALKOLE BAĞLI OLMAYAN YAĞLI KARACİĞER HASTALIĞININ PROGRESYONUNU ARTTIRMADI

Year 2021, , 360 - 368, 31.07.2021
https://doi.org/10.26650/IUITFD.2021.849531

Abstract

Amaç: Vitamin D antioksidan, antiinflamatuvar ve antiglikasyon etkinliğe ve karaciğeri koruyucu potansiyele sahiptir. Vitamin D eksikliği/yetersizliği (VDD/VDI) ile karaciğer bozukluklarının ciddiyeti arasında bir ilişki bulunmaktadır. VDD’nin alkole bağlı olmayan yağlı karaciğer hastalığının (NAFLD) progresyonunda etkili olduğu bildirilmiştir. Fakat deneysel sonuçlar yeterli değildir. Bu nedenle, bu çalışmada VDD’nin yüksek fruktozlu (HFr) içme suyu uygulanarak oluşturulan NAFLD üzerine etkisi incelendi. Gereç ve Yöntemler: Erkek Wistar sıçanlar kontrol, HFr, VDD+Fr ve VDD olmak üzere 4 gruba ayrıldı. Kontrol ve HFr grupları Vit D3 içeren, diğerleri ise Vit D3 içermeyen yemle 12 hafta beslendiler. HFr (%30; w/v) içme suyu ile son 8 hafta uygulandı. İnsulin direnci (IR), serum lipitleri, hepatik trigliserit, lipit peroksit, protein karbonil, ileri glikasyon ürünleri (AGEs) ve inflamasyon (TNF-α ve miyeloperoksidaz) göstergeleri tayin edildi. Bulgular: HFR ve VDD+HFr gruplarında serumda transaminazlar arttı, hipertrigliseridemi, ve insülin direnci oluştu. Her iki grupta da karaciğerde trigliserit düzeyleri, lipit ve protein oksidasyon ürünleri, protein glikasyon ve inflamasyon göstergeleri arttı, mikroveziküler steatoz ve hepatosit balonlaşması saptandı. IR ve inflamasyon göstergeleri VDD+HFr grubunda daha yüksek olmasına rağmen, iki grup arasında serum transaminazları, karaciğer trigliserit, lipit ve protein oksidasyon ürünleri ve glikasyon göstergeleri düzeylerinde bir farklılık bulunmadı. Ancak Nrf2 mRNA ekspresyonu ile süperoksit dismutaz ve glutatyon peroksidazın mRNA ekspresyonları ve aktivitelerinin VDD+HFr grubunda daha yüksek olduğu bulundu. Sonuç: Sonuçlarımız VDD’nin HFr ile oluşturulan karaciğer hasarı ve glikooksidatif streste bir değişiklik oluşturmadığını göstermektedir.

Supporting Institution

İstanbul Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi

Project Number

TSA-2018-30443

References

  • 1. Ibrahim MA, Kelleni M, Geddawy A. Nonalcoholic fatty liver disease: Current and potential therapies. Life Sci 2013;92(2):114-8. [CrossRef]
  • 2. Fernando DH, Forbe JM, Angus PW, Herath CB. Development and progression of non-alcoholic fatty liver disease: The role of advanced glycation end products. Int J Mol Sci 2019;20(20):5037. [CrossRef]
  • 3. Alwahsh SM, Gebhardt R. Dietary fructose as a risk factor for non-alcoholic fatty liver disease (NAFLD). Arch Toxicol 2017;91(4):1545-63. [CrossRef]
  • 4. Takahashi Y, Soejima Y, Fukusato T. Animal models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. World J Gastroenterol 2012;18(19):2300-8. [CrossRef]
  • 5. Jegatheesan P, De Bandt JP. Fructose and NAFLD: Multifaceted aspects of fructose metabolism. Nutrients 2017;9(3):230. [CrossRef]
  • 6. Gugliucci A. Formation of fructose-mediated advanced glycation end products and their roles in metabolic and inflammatory diseases. Adv Nutr 2017;8(1):54-62. [CrossRef]
  • 7. Kwok RM, Torres DM, Harrison SA. Vitamin D and nonalcoholic fatty liver disease (NAFLD): Is it more than just an association? Hepatology 2013;58(3):1166-74. [CrossRef]
  • 8. Uberti F, Morsanuto V, Molinari C. Vitamin D in oxidative stress and diseases. ‘A Critical Evaluation of Vitamin D-Basic Overview. Ed: Sivakumar Joghi Thatha Gowder, IntechOpen, Chapter 2, pp 47-73. 2017. [CrossRef]
  • 9. Kheirouri S, Alizadeh M. Vitamin D and advanced glycation end products and their reseptors. Pharmacol Res 2020;158:104879. [CrossRef]
  • 10. Khan S, Ali A, Khan S, Bakillah A, Damanhouri G, Khan A, et al. Current therapies in alleviating liver disorders and cancers with a special focus on the potential of vitamin D. Nutr Metab 2018;15:13. [CrossRef]
  • 11. Eliades M, Spyrou E. Vitamin D: A new player in nonalcoholic fatty liver disease? World J Gastroenterol 2015;21(6):1718-27. [CrossRef]
  • 12. Berridge MJ. Vitamin D signalling in health and disease. Biochem Biophys Res Commun 2015;460(1):53-71. [CrossRef]
  • 13. Wang H, Chen W, Li D, Yin X, Zhang X, Olsen N, et al. Vitamin D and chronic diseases. Aging Dis 2017;8(3):346-53. [CrossRef]
  • 14. Wimalawansa SJ. Vitamin D deficiency: Effects on oxidative stress, epigenetics, gene regulation and aging. Biology 2019;8(2):30-45. [CrossRef]
  • 15. Institute of Medicine. Dietary references intakes for calcium and vitamin D. Eds: Ross AC, Taylor CL, Yaktine AL, Del Valle HB, Washington-DC, National Academies Press (US), 2011.
  • 16. Elangovan H, Chahal S, Gunton JE. Vitamin D in liver disease: Current evidence and potential directions. Biochim Biophys Acta 2017;1863(4):907-16. [CrossRef]
  • 17. Karatayli E, Stokes CS, Lammert F. Vitamin D in preclinical models of fatty liver disease. Anticancer Res 2020;40(1): 527-34. [CrossRef]
  • 18. Rachmilewitz D, Stamler JS, Karmeli F, Mullins ME, Singel DJ, Loscalzo J, et al. “Peroxynitrite-induced rat colitis - a new model of colonic inflammation”. Gastroenterology 1993;105(6):1681-8. [CrossRef]
  • 19. Wang H, Joseph JA. Quantifying cellular oxidative stress by dichlorofluorescein assay using microplate reader. Free Radic Biol Med 1999;27(5-6):612-6. [CrossRef]
  • 20. Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzymol 1978;52:302-10. [CrossRef]
  • 21. Reznick AZ, Packer L. Oxidative damage to proteins: spectrophotometric method for carbonyl assay. Methods Enzymol 1994;233:357-63. [CrossRef]
  • 22. Hanasand M, Omdal R, Norheim KB, Gøransson LG, Brede C, Johnson G. Improved detection of advanced oxidation protein products in plasma. Clin Chim Acta 2012;413(9- 10):901-6. [CrossRef]

VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS

Year 2021, , 360 - 368, 31.07.2021
https://doi.org/10.26650/IUITFD.2021.849531

Abstract

Objective: Vitamin D has antioxidant, anti-inflammatory and antiglycation activities, and hepatoprotective potential. There is a relationship between vitamin D deficiency (VDD) and the severity of liver disorders. VDD has been proposed to contribute to the progression of nonalcoholic fatty liver disease (NAFLD). However, experimental results are not clear. Therefore, in this study, the effects of a VDD diet on high fructose (HFr) drinking-induced NAFLD was evaluated. Material and Method: Male Wistar rats were divided into four groups as control, HFr, VDD+HFr, and VDD. Control and HFr groups were fed a control diet, and other groups with a VDD-diet for 12 weeks. HFr (30%; w/v; in drinking water) was given in the last 8 weeks. Insulin resistance (IR), serum lipids, hepatic triglyceride, lipid peroxide, protein carbonyl, advanced glycation end products (AGEs) and inflammation (TNF-α and myeloperoxidase) parameters, and histopathological changes were investigated. Results: Increases in serum transaminases, hypertriglyceridemia, and IR were observed in HFr and VDD+HFr groups. Increased liver triglyceride, lipid and protein oxidation products, protein glycation and inflammation markers as well as microvesicular hepatic steatosis and hepatocyte ballooning were observed in both groups. Although IR and hepatic inflammation markers were higher in the VDD+HFr group, serum transaminases, hepatic triglyceride, lipid and protein oxidation products, and glycation indicators in the liver did not alter between the two groups. However, Nrf2 mRNA expression and superoxide dismutase and glutathione peroxidase mRNA expression and activities were significantly higher in the VDD+HFr group. Conclusion: Our results show that VDD did not augmented HFr-induced hepatotoxicity and glycooxidative stress in the liver of rats.

Project Number

TSA-2018-30443

References

  • 1. Ibrahim MA, Kelleni M, Geddawy A. Nonalcoholic fatty liver disease: Current and potential therapies. Life Sci 2013;92(2):114-8. [CrossRef]
  • 2. Fernando DH, Forbe JM, Angus PW, Herath CB. Development and progression of non-alcoholic fatty liver disease: The role of advanced glycation end products. Int J Mol Sci 2019;20(20):5037. [CrossRef]
  • 3. Alwahsh SM, Gebhardt R. Dietary fructose as a risk factor for non-alcoholic fatty liver disease (NAFLD). Arch Toxicol 2017;91(4):1545-63. [CrossRef]
  • 4. Takahashi Y, Soejima Y, Fukusato T. Animal models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. World J Gastroenterol 2012;18(19):2300-8. [CrossRef]
  • 5. Jegatheesan P, De Bandt JP. Fructose and NAFLD: Multifaceted aspects of fructose metabolism. Nutrients 2017;9(3):230. [CrossRef]
  • 6. Gugliucci A. Formation of fructose-mediated advanced glycation end products and their roles in metabolic and inflammatory diseases. Adv Nutr 2017;8(1):54-62. [CrossRef]
  • 7. Kwok RM, Torres DM, Harrison SA. Vitamin D and nonalcoholic fatty liver disease (NAFLD): Is it more than just an association? Hepatology 2013;58(3):1166-74. [CrossRef]
  • 8. Uberti F, Morsanuto V, Molinari C. Vitamin D in oxidative stress and diseases. ‘A Critical Evaluation of Vitamin D-Basic Overview. Ed: Sivakumar Joghi Thatha Gowder, IntechOpen, Chapter 2, pp 47-73. 2017. [CrossRef]
  • 9. Kheirouri S, Alizadeh M. Vitamin D and advanced glycation end products and their reseptors. Pharmacol Res 2020;158:104879. [CrossRef]
  • 10. Khan S, Ali A, Khan S, Bakillah A, Damanhouri G, Khan A, et al. Current therapies in alleviating liver disorders and cancers with a special focus on the potential of vitamin D. Nutr Metab 2018;15:13. [CrossRef]
  • 11. Eliades M, Spyrou E. Vitamin D: A new player in nonalcoholic fatty liver disease? World J Gastroenterol 2015;21(6):1718-27. [CrossRef]
  • 12. Berridge MJ. Vitamin D signalling in health and disease. Biochem Biophys Res Commun 2015;460(1):53-71. [CrossRef]
  • 13. Wang H, Chen W, Li D, Yin X, Zhang X, Olsen N, et al. Vitamin D and chronic diseases. Aging Dis 2017;8(3):346-53. [CrossRef]
  • 14. Wimalawansa SJ. Vitamin D deficiency: Effects on oxidative stress, epigenetics, gene regulation and aging. Biology 2019;8(2):30-45. [CrossRef]
  • 15. Institute of Medicine. Dietary references intakes for calcium and vitamin D. Eds: Ross AC, Taylor CL, Yaktine AL, Del Valle HB, Washington-DC, National Academies Press (US), 2011.
  • 16. Elangovan H, Chahal S, Gunton JE. Vitamin D in liver disease: Current evidence and potential directions. Biochim Biophys Acta 2017;1863(4):907-16. [CrossRef]
  • 17. Karatayli E, Stokes CS, Lammert F. Vitamin D in preclinical models of fatty liver disease. Anticancer Res 2020;40(1): 527-34. [CrossRef]
  • 18. Rachmilewitz D, Stamler JS, Karmeli F, Mullins ME, Singel DJ, Loscalzo J, et al. “Peroxynitrite-induced rat colitis - a new model of colonic inflammation”. Gastroenterology 1993;105(6):1681-8. [CrossRef]
  • 19. Wang H, Joseph JA. Quantifying cellular oxidative stress by dichlorofluorescein assay using microplate reader. Free Radic Biol Med 1999;27(5-6):612-6. [CrossRef]
  • 20. Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzymol 1978;52:302-10. [CrossRef]
  • 21. Reznick AZ, Packer L. Oxidative damage to proteins: spectrophotometric method for carbonyl assay. Methods Enzymol 1994;233:357-63. [CrossRef]
  • 22. Hanasand M, Omdal R, Norheim KB, Gøransson LG, Brede C, Johnson G. Improved detection of advanced oxidation protein products in plasma. Clin Chim Acta 2012;413(9- 10):901-6. [CrossRef]
There are 22 citations in total.

Details

Primary Language English
Subjects Health Care Administration
Journal Section RESEARCH
Authors

İlknur Bingül 0000-0002-6432-3541

Canan Kucukgergin 0000-0002-1797-5889

Fatih Aydın 0000-0002-3336-4332

Işın Doğan Ekici This is me 0000-0003-4062-9519

Semra Dogru Abbasoglu 0000-0003-3467-9763

Mujdat Uysal 0000-0002-8802-8766

Project Number TSA-2018-30443
Publication Date July 31, 2021
Submission Date December 29, 2020
Published in Issue Year 2021

Cite

APA Bingül, İ., Kucukgergin, C., Aydın, F., Doğan Ekici, I., et al. (2021). VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS. Journal of Istanbul Faculty of Medicine, 84(3), 360-368. https://doi.org/10.26650/IUITFD.2021.849531
AMA Bingül İ, Kucukgergin C, Aydın F, Doğan Ekici I, Dogru Abbasoglu S, Uysal M. VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS. İst Tıp Fak Derg. July 2021;84(3):360-368. doi:10.26650/IUITFD.2021.849531
Chicago Bingül, İlknur, Canan Kucukgergin, Fatih Aydın, Işın Doğan Ekici, Semra Dogru Abbasoglu, and Mujdat Uysal. “VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS”. Journal of Istanbul Faculty of Medicine 84, no. 3 (July 2021): 360-68. https://doi.org/10.26650/IUITFD.2021.849531.
EndNote Bingül İ, Kucukgergin C, Aydın F, Doğan Ekici I, Dogru Abbasoglu S, Uysal M (July 1, 2021) VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS. Journal of Istanbul Faculty of Medicine 84 3 360–368.
IEEE İ. Bingül, C. Kucukgergin, F. Aydın, I. Doğan Ekici, S. Dogru Abbasoglu, and M. Uysal, “VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS”, İst Tıp Fak Derg, vol. 84, no. 3, pp. 360–368, 2021, doi: 10.26650/IUITFD.2021.849531.
ISNAD Bingül, İlknur et al. “VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS”. Journal of Istanbul Faculty of Medicine 84/3 (July 2021), 360-368. https://doi.org/10.26650/IUITFD.2021.849531.
JAMA Bingül İ, Kucukgergin C, Aydın F, Doğan Ekici I, Dogru Abbasoglu S, Uysal M. VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS. İst Tıp Fak Derg. 2021;84:360–368.
MLA Bingül, İlknur et al. “VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS”. Journal of Istanbul Faculty of Medicine, vol. 84, no. 3, 2021, pp. 360-8, doi:10.26650/IUITFD.2021.849531.
Vancouver Bingül İ, Kucukgergin C, Aydın F, Doğan Ekici I, Dogru Abbasoglu S, Uysal M. VITAMIN D DEFICIENCY DID NOT AUGMENT THE PROGRESSION OF HIGH-FRUCTOSE-INDUCED NONALCOHOLIC FATTY LIVER DISEASE IN RATS. İst Tıp Fak Derg. 2021;84(3):360-8.

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