PROTO-HORMONES LEVELS OF ADIPOSE TISSUE, INTERLEUKIN-6 AND INDICATORS OF DETOXIFYING FUNCTION OF THE LIVER IN PATIENTS WITH HYPERTENSION AND OBESITY COMBINED WITH NON-ALCOHOLIC FATTY LIVER DISEASE
Abstract
The research estimates the state of liver detoxifying function and analyzes the changes in the levels of leptin, adiponectin and interleukin-6 in patients with arterial hypertension in combination with obesity and non-alcoholic fatty liver disease.
Aim. The aim of the study is to evaluate levels of proto-hormones adipose tissue, interleukin-6 and indicators of detoxifying function of the liver in patients with hypertension and obesity combined with non-alcoholic fatty liver disease (NAFLD).
Materials and methods. The study involved patients with arterial hypertension combined with obesity and NAFLD. All patients underwent anthropometric, general clinical, laboratory (blood lipid profile) and instrumental diagnostics (electrocardiography, echocardiography, ultrasonography, 13C-metacetin breath test, ELISA (adiponectin, leptin, IL-6). The patients’ height and weight were measured, the body mass index was calculated according to standard formulas.
Results. Patients with arterial hypertension combined with obesity and NAFLD at the stage of steatohepatitis showed an increase in the levels of leptin and IL-6 and a decrease in the level of adiponectin. This group also revealed a moderate decrease in liver detoxifying function, as indicated by the results of 13C- MBT due to a 46.7 % decrease in the metabolic rate and a decrease in cumulative doses of CUM40 by 40 % and CUM120 by 46.8 %, respectively.
Conclusions. The elevated levels of leptin and IL-6 and lowered adiponectin levels can be used to determine the degree of activity of non-alcoholic steatohepatitis and predict the course of NAFLD in combination with hypertension and obesity.
An increased level of leptin and IL-6 and a low level of adiponectin in patients with such a comorbid pathology lead to an increase in the left ventricular myocardial mass index and aggravate the course of arterial hypertension.
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References
Adolph, T. E., Grander, C., Grabherr, F., Tilg, H. (2017). Adipokines and non-alcoholic fatty liver disease: multiple interactions. International Journal of Molecular Sciences, 18 (8), 1649. doi: http://doi.org/10.3390/ijms18081649
Kumar, R., Prakash, S., Chhabra, S., Singla, V., Madan, K., Datta Gupta, S. et. al. (2012). Association of pro-inflammatory cytokines, adipokines & oxidative stress with insulin resistance & non-alcoholic fatty liver disease. Indian Journal of Medical Research, 136 (2), 229–236.
Polyzos, S. A., Kountouras, J., Zavos, C., Tsiaousi, E. (2010). The role of adiponectin in the pathogenesis and treatment of non-alcoholic fatty liver disease. Diabetes, Obesity and Metabolism, 12 (5), 365–383. doi: http://doi.org/10.1111/j.1463-1326.2009.01176.x
Fang, H., Judd, R. L. (2018). Adiponectin Regulation and Function. Comprehensive Physiology, 8 (3), 1031–1063. doi: http://doi.org/10.1002/cphy.c170046
Andrabi, K., Dar, R., Rasool, S., Waza, A., Ayoub, G., Qureshi, M. et. al. (2019). Polymorphic analysis of leptin promoter in obese/diabetic subjects in Kashmiri population. Indian Journal of Endocrinology and Metabolism, 23 (1), 111. doi: http://doi.org/10.4103/ijem.ijem_164_18
Lemoine, M., Ratziu, V., Kim, M., Maachi, M., Wendum, D., Paye, F. et. al. (2009). Serum adipokine levels predictive of liver injury in non-alcoholic fatty liver disease. Liver International, 29 (9), 1431–1438. doi: http://doi.org/10.1111/j.1478-3231.2009.02022.x
Procaccini, C., Galgani, M., De Rosa, V., Carbone, F., La Rocca, C., Ranucci, G. et. al. (2010). Leptin: The Prototypic Adipocytokine and its Role in NAFLD. Current Pharmaceutical Design, 16 (17), 1902–1912. doi: http://doi.org/10.2174/138161210791208884
Ghantous, C. M., Azrak, Z., Hanache, S., Abou-Kheir, W., Zeidan, A. (2015). Differential Role of Leptin and Adiponectin in Cardiovascular System. International Journal of Endocrinology, 2015, 1–13. doi: http://doi.org/10.1155/2015/534320
Barrios, V., Escobar, C., Calderon, A., Böhm, M. (2009). Blood pressure goal achievement with olmesartan medoxomil-based treatment: additional analysis of the OLMEBEST study. Vascular Health and Risk Management, 5, 723. doi: http://doi.org/10.2147/vhrm.s7003
Hashizume, M., Mihara, M. (2011). IL-6 and lipid metabolism. Inflammation and Regeneration, 31 (3), 325–333. doi: http://doi.org/10.2492/inflammregen.31.325
Chalasani, N., Younossi, Z., Lavine, J. E., Diehl, A. M., Brunt, E. M., Cusi, K. et. al. (2012). The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. Hepatology, 55 (6), 2005–2023. doi: http://doi.org/10.1002/hep.25762
Gorowska-Kowolik, K., Chobot, A., Kwiecien, J. (2017). 13C Methacetin Breath Test for Assessment of Microsomal Liver Function: Methodology and Clinical Application. Gastroenterology Research and Practice, 2017, 1–5. doi: http://doi.org/10.1155/2017/7397840
Park, G. J.-H., Wiseman, E., George, J., Katelaris, P. H., Seow, F., Fung, C., Ngu, M. C. (2011). Non-invasive Estimation of Liver Fibrosis in Non-alcoholic Fatty Liver Disease Using the 13C-Caffeine Breath Test. Journal of Gastroenterology and Hepatology, 26 (9), 1411. doi: http://doi.org/10.1111/j.1440-1746.2011.06760.x
Bochar, O., Sklyarov, E., Bochar, V. (2017). Leptin and interleukin-6 level in patients with hypertension and obesity combined with non-alcoholic steatohepatitis during treatment with sartans and statins. Current Issues in Pharmacy and Medical Sciences, 30 (2), 57–60. doi: http://doi.org/10.1515/cipms-2017-0011
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