UDC

577.151.63+577.126

DOI

10.37482/2687-1491-Z202

Authors

Svetlana V. Notova* ORCID: https://orcid.org/0000-0002-6378-4522
Olga V. Marshinskaia* ORCID: https://orcid.org/0000-0002-5611-5128
Tatiana V. Kazakova* ORCID: https://orcid.org/0000-0003-3717-4533
*Orenburg State University (Orenburg, Russia)

Corresponding author: Olga Marshinskaia, address: prosp. Pobedy 13, Orenburg, 460018, Russia; e-mail: m.olja2013@yandex.ru

Abstract

Over the last decades, the dietary pattern of the population has undergone changes, including a significant increase in the consumption of high-calorie food. The purpose of this study was to investigate the activity of antioxidant enzymes in rats with and without genetic predisposition to cardiovascular disease eating a high-calorie diet. Materials and мethods. Wistar (n = 30) and SHR rats (n = 30; predisposed to cardiovascular disease) were used. Animals of both strains were subdivided into two groups: control (basic diet) and experimental (high-calorie diet). Parameters of carbohydrate and lipid metabolism were determined using a biochemistry analyser; haematological analysis was performed in order to establish the type of nonspecific adaptive response of the body. The state of the antioxidant system was evaluated using the animals’ blood serum and liver homogenate by determining catalase, superoxide dismutase and glutathione peroxidase activity. Results. High-calorie diet led to excessive body weight, changes in lipid profile, impaired glucose tolerance and inadequate adaptive response of the functional systems (manifested in the strain on the adaptive mechanisms and maladaptation) as well as to depletion of antioxidant enzymes in rats of both experimental groups. The parameters of animals with and without genetic predisposition to cardiovascular disease were found to be virtually identical. Despite the fact that genetic factors contribute significantly to the development of metabolic pathologies, the results obtained in the group of Wistar rats confirm that excessive caloric intake is one of the major causes of metabolic disorders.

Keywords

high-calorie diet, overweight, antioxidant defence system, catalase, superoxide dismutase, glutathione peroxidase, genetic predisposition to cardiovascular disease

References

1. Kodentsova V.M., Vrzhesinskaya O.A., Risnik D.V., Nikityuk D.B., Tutelyan V.A. Micronutrient Status of Population of the Russian Federation and Possibility of Its Correction. State of the Problem. Probl. Nutr., 2017, vol. 86, no. 4, pp. 113–124 (in Russ.). https://doi.org/10.24411/0042-8833-2017-00067
2. Hruby A., Hu F.B. The Epidemiology of Obesity: A Big Picture. PharmacoEconomics, 2015, vol. 33, no. 7, pp. 673–689. https://doi.org/10.1007/s40273-014-0243-x
3. Muoio D.M. Metabolic Inflexibility: When Mitochondrial Indecision Leads to Metabolic Gridlock. Cell, 2014, vol. 159, no. 6, pp. 1253–1262. https://doi.org/10.1016/j.cell.2014.11.034
4. Knaus U.G. Oxidants in Physiological Processes. Schmidt H.H.H.W., Ghezzi P., Cuadrado A. (eds.). Reactive Oxygen Species: Network Pharmacology and Therapeutic Applications. Cham, 2021, pp. 27–47. https://doi.org/10.1007/164_2020_380
5. Chao H.-W., Chao S.-W., Lin H., Ku H.-C., Cheng C.-F. Homeostasis of Glucose and Lipid in Non-Alcoholic Fatty Liver Disease. Int. J. Mol. Sci., 2019, vol. 20, no. 2. Art. no. 298. https://doi.org/10.3390/ijms20020298
6. Heianza Y., Qi L. Gene-Diet Interaction and Precision Nutrition in Obesity. Int. J. Mol. Sci., 2017, vol. 18, no. 4. Art. no. 787. https://doi.org/10.3390/ijms18040787
7. Cordain L., Eaton S.B., Sebastian A., Mann N., Lindeberg S., Watkins B.A., O’Keefe J.H., Brand-Miller J. Origins and Evolution of the Western Diet: Health Implications for the 21st Century. Am. J. Clin. Nutr., 2005, vol. 81, no. 2, pp. 341–354. https://doi.org/10.1093/ajcn.81.2.341
8. Jagannathan R., Neves J.S., Dorcely B., Chung S.T., Tamura K., Rhee M., Bergman M. The Oral Glucose Tolerance Test: 100 Years Later. Diabetes Metab. Syndr. Obes., 2020, vol. 13, pp. 3787–3805. https://doi.org/10.2147/DMSO.S246062
9. Klop B., Elte J.W.F., Cabezas M.C. Dyslipidemia in Obesity: Mechanisms and Potential Targets. Nutrients, 2013, vol. 5, no. 4, pp. 1218–1240. https://doi.org/10.3390/nu5041218
10. Notova S.V., Kvan O.V., Miroshnikov S.V. Osobennosti elementnogo statusa pri nekotorykh nespetsificheskikh reaktsiyakh adaptatsii (povyshennoy aktivatsii i pereaktivatsii) [Elemental Status Features During Some Unspecific Adaptation Reactions (Abnormally High Activation and Reactivation)]. Vestnik OGU, 2011, vol. 134, no. 15, pp. 88–90.
11. Clyburn C., Carson K.E., Smith C.R., Travagli R.A., Browning K.N. Brainstem Astrocytes Control Homeostatic Regulation of Caloric Intake. J. Physiol., 2023, vol. 601, no. 4, pp. 801–829. https://doi.org/10.1113/JP283566
12. Carocho M., Ferreira I.C.F.R. A Review on Antioxidants, Prooxidants and Related Controversy: Natural and Synthetic Compounds, Screening and Analysis Methodologies and Future Perspectives. Food Chem. Toxicol., 2013, vol. 51, pp. 15–25. https://doi.org/10.1016/j.fct.2012.09.021
13. Prince M.R.U., Zihad S.M.N.K., Ghosh P., Sifat N., Rouf R., Al Shajib G.M., Alam M.A., Shilpi J.A., Uddin S.J. Amaranthus spinosus Attenuated Obesity-Induced Metabolic Disorders in High-Carbohydrate-High-Fat Diet-Fed Obese Rats. Front. Nutr., 2021, vol. 8. Art. no. 653918. https://doi.org/10.3389/fnut.2021.653918