Biochemical markers of liver damage with a fructose-induced diet in rats


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

Relevance. The increased content of fructose as a common source of carbohydrates in foods leads to metabolic disorders in the body, which may be due to biochemical characteristics of fructose metabolism. The result is an increased risk of obesity, diabetes mellitus, cardiovascular diseases, as well as liver diseases induced by the formation of oxidative stress amid changes in lipid and carbohydrate metabolism. The destructive processes in the liver may be indicated by an increase in the content of the main markers of hepatocyte cytolysis: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH). Objective. To create an experimental model of the development of inflammatory processes in the liver under the influence of a fructose-induced diet. Material and methods. The study was conducted on 50 male rats with a body weight of 250-300 g. Animals were divided into experimental and control groups of 25 animals each. Rats of the control group received a balanced diet of vivarium, animals of the experimental group received a diet containing 60% fructose of daily calories. On the 60th day, the formation of metabolic deviations in the long-term was evaluated. In the obtained serum, the content of glucose, cholesterol (cholesterol), low-density lipoproteins (LDL), triglycerides (TG), insulin, the activity of ALT, AST, alkaline phosphatase, LDH were studied. Biochemical studies were carried out on an automatic analyzer AU-480 (Beckman Coulter, USA) using reagents of the same manufacturer. The insulin content was determined on an enzyme-linked immunosorbent analyzer StatFax-2100 (Awareness Technology, USA) using a set of reagents LLC Vector-best, Russia. Indices of insulin resistance were calculated. Results. During the study, there was a tendency to an increase in glucose concentration with a significant increase on the 21st and 60th day of the experiment by 1.18 and 1.21 times, respectively, and cholesterol on the 35th day of the experiment by 1.59 times relative to the control in rat blood serum. The insulin concentration significantly increased throughout the experiment, exceeding the control values by 1.5, 1.7, and 1.9 times on the 21st, 35th, and 60th days of the experiment. The insulin resistance indices also differed from the control values, which may indicate the formation of insulin resistance. The LDL content was statistically significantly increased throughout the experiment. During the experiment, there was an increase in the activity of hepatocyte cytolysis markers with a significant increase compared with the control. A decrease in the de Ritis coefficient confirms the activation of cytolytic processes in the liver. Conclusion. Thus, a fructose-induced diet increases the content of specific rat liver enzymes (ALT, AST, ALP, LDH) against the background of disturbances in lipid and carbohydrate metabolism with increased concentrations of cholesterol, triglycerides, LDL, as well as glucose and insulin, the formation of insulin resistance. The reason for the initiation of cytolytic processes in hepatocytes may be free-radical oxidation of protein-lipid complexes and activation of inflammatory reactions as a result of increased consumption of fructose.

Full Text

Restricted Access

About the authors

O. G Gileva

Izhevsk State Medical Academy

Email: kld.igma@mail.ru
Post-graduate Student, Department of Clinical Biochemistry and Laboratory Diagnostics Izhevsk

References

  1. Долгов В.В. Клиническая лабораторная диагностика: Национальное руководство. М.: ГЭОТАР-Медиа, 2017; 808.
  2. Павлова З.Ш., Голодников И.И., Камалов А.А. Биохимические механизмы развития неалкогольной жировой бо лезни печени под воздействием фруктозы. Технологии живых систем. 2018; 15: 18-27.
  3. Решетняк М.В., Хирманов В.Н., Зыбина Н.Н. Модель метаболического синдрома, вызванного кормлением фруктозой: патогенетические взаимосвязи обменных нарушений. Медицинский академический журнал. 2011; 11: 23-27.
  4. Лещенко Д.В., Костюк Н.В. Диетически индуцированные животные модели метаболического синдрома. Верхневолжский медицинский журнал. 2015; 14: 34-39.
  5. Kleiner D.E., Makhlouf H.R. Histilogy of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis in Adult and Children. Clin Liver Dis. 2016; 20(2): 293-312.
  6. Lankin V.Z., Konovalova G.G., Tikhaze A.K., Shumaev K.B., Kumskova E.M., Viigimaa M. The Initiation of the Free Radical Peroxidation of Low Density Lipoproteins by Glucose and Its Metabolity Methylglyoxal: a Common Molecular Mechanismof Vascular Wall Injure in Atherosclerosis and Diabetes. Mol. Cell. Bichem. 2014; 395: 241-252.
  7. Медведев И.Н. Динамика нарушений внутрисосудистой активности тромбоцитов у крыс в ходе формирования метаболического синдрома с помощью фруктозной модели. Вопросы питания. 2016; 85: 42-46.
  8. Lim J.S. et al. The role of fructose in the pathogenesis of nonalcoholic fatty liver disease and the metabolic syndrome. Nat. Rev. Gastroenterol. Hepatol. 2010; 5: 251-264.
  9. Syaoyan Chu, Kirgizova O.Yu. Metabolic syndrome: some results and prospects for solving the problem. Byulleten' VSNC SO RAMN. 2016; 1: 187-194.

Supplementary files

Supplementary Files
Action
1. JATS XML

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies