Journals / Turkish Journal of Gastroenterology / 2016 / Cilt: 27 - Sayı: 4

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease LIVER

Pages
361–366
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These data show that NAFLD patients with IR may have increased risk for disease progression

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Oxidative stress and insulin resistance (IR) are major contributors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD).
📊
Key Findings & Data:Materials and Methods: Thirty-two patients with no alcohol intake and biopsy-proven diagnosis of NAFLD were studied (M/F: 17/15; mean age 46.5±11.4 years).
💡
Conclusion & Impact:These data show that NAFLD patients with IR may have increased risk for disease progression
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Oxidative stress and insulin resistance (IR) are major contributors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The purpose of this study was to find the relation between oxidative stress parameters and histopathological findings in NAFLD patients with and without insulin resistance (IR). Materials and Methods: Thirty-two patients with no alcohol intake and biopsy-proven diagnosis of NAFLD were studied (M/F: 17/15; mean age 46.5±11.4 years). Twenty-one NAFLD patients with IR were compared with 11 patients without IR. The fasting insulin level was measured, and the insulin resistance index was calculated using the homeostasis model assessment (HOMA) method. Malondialdehyde (MDA) and superoxide dismutase (SOD) activities were measured in tissue and serum specimens. Glutathione (GH) was measured in tissue homogenates. Nitric oxide (NO), vitamin E and C levels were measured in serum. Results: Patients with IR had significantly higher tissue MDA levels (p=0.001) and significantly decreased tissue SOD and GH levels (p=0.001 and 0.002, respectively) than those without IR. The steatosis grade, necroinflammatory grade and stage were significantly higher in patients with IR (p=0.035, 0.003 and 0.001, respectively). HOMA IR significantly correlated with the necroinflammatory grade, stage, tissue MDA, SOD and GH (p=0.013, 0.001, 0.008, 0.001 and 0.001, respectively). Serum MDA (?=1.88, p=0.002), serum SOD (?=0.57, p=0.006), tissue MDA (?=0.22, p=0.006), tissue SOD (?=1.48, p=0.071) and stage (?=2.81, p=0.003) were independently associated with increased HOMA IR. Increased MDA [OR: 1.51; 95% CI: (1.03-2.22); p=0.034] was a risk factor for nonalcoholic steatohepatitis (NASH), and increased SOD activity had a preventive effect against NASH [OR: 0.008; 95% CI: (0.001-0.98); p=0.04]. Conclusion: This study shows that insulin resistance in NAFLD correlates with enhanced oxidative stress. Histopathological disease severity significantly correlated with oxidative stress parameters. These data show that NAFLD patients with IR may have increased risk for disease progression

🔖

Cite This Article

KÖROĞLU, E., CANBAKAN, İ. B., ATAY, K., HATEMİ, A. İ., TUNCER, M. M., DOBRUCALI, A., SONSUZ, A., GÜLTEPE, İ., ŞENTÜRK, H. (2016). Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease LIVER. Turkish Journal of Gastroenterology, Cilt: 27 - Sayı: 4, 361–366. https://ajindex.com/articles/409371

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (3)

  1. Malhi H, Gores GJ. Molecular mechanisms of lipotoxicity in nonalco- holic fatty liver disease. Semin Liver Dis 2008; 28: 360-9. [CrossRef] Browning DJ, Horton JD. Molecular mediators of hepatic steatosis and liver injury. J Clin Invest 2004; 114: 147-52. [CrossRef] Bergamini CM, Gambetti S, Dondi A, Cervellati C. Oxygen, re- active oxygen species and tissue damage. Curr Pharm Des 2004;10:1611-26. [CrossRef] Sanyal AJ, Campbell SC, Mirshahi F, et al. Nonalcoholic steatohep- atitis: association of insulin resistance and mitochondrial abnor- malities. Gastroenterology 2001; 120: 1183-92. [CrossRef] Chalasani N, Deeg MA, Crabb DW. Systemic levels of lipid peroxida- tion and its metabolic and dietary correlates in patients with non- alcoholic steatohepatitis. Am J Gastroenterol 2004; 99: 1497-502. [CrossRef] Yesilova Z, Yaman H, Oktenli C, et al. Systemic markers of lipid peroxidation and antioxidants in patients with non-alcoholicfatty liver disease. Am J Gastroenterol 2005; 100: 850-5. [CrossRef] Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. Am J Gastroenterol 1999; 94: 2467-74. [CrossRef] Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzy- mol 1978; 52: 302-10. [CrossRef] Sun Y, Oberley LW, Li Y. A simple method for clinical assay of su- peroxide dismutase. Clin Chem 1988; 34: 497-500.
  2. Beutler E, Duron O, Kelly BM. Improved method for the determi- nation of blood glutathione. J Lab Clin Med 1963; 61: 882-8.
  3. Omaye ST, Turnbull JD, Sauberlich HE. Selected methods for the determination of ascorbic acid in animal cells, tissues and fluids. Method Enzymol 1979; 6: 3-13. [CrossRef] Maritim AC, Sanders RA, Watkins JB 3rd. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol 2003; 17: 24-38. [CrossRef] Sundaram SS, Zeitler P, Nadeau K. The metabolic syndrome and nonalcoholic fatty liver disease in children. Curr Opin Pediatr 2009; 21: 529-35. [CrossRef] Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steato- sis to cirrhosis. Hepatology 2006; 43: S99-S112. [CrossRef] Cohen JC, Horton JD, Hobbs HH. Human fatty liver disease: old ques- tions and new insights. Science 2011; 332: 1519-23. [CrossRef] Leach NV, Dronca E, Vesa SC, et al. Serum homocysteine levels, oxidative stress and cardiovascular risk in non-alcoholic steato- hepatitis Eur J Int Med 2014; 25: 762-7. Diez-Rodriquez R. Insulin resistance and