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Abstract
Not only obesity/overweight and type 2 diabetes, but also hypothyroidism (HT), polycystic ovary syndrome (PCOS), hypogonadism, and hormone deficiency are associated with the hormone-centric theory of the pathogenesis of metabolic dysfunction-related steatotic liver disease (MDSLD). MDSLD is often associated with hypothyroidism, polycystic ovary syndrome, hypogonadism, and growth hormone deficiency. It has specific mechanisms of progression, which lead to metabolic background deterioration. Such MDSLD quickly progresses to cirrhosis, which requires the doctors attention. Lifestyle changes and hormone
replacement therapy reduce liver lipid infiltration (except for growth hormone deficiency). Information about MDSLD is ambiguous, what determined the expediency of our research. The aim of the work: to characterize the features of the MDSLD in HT and to explain their leading mechanisms. Material and methods. 36 examined patients with arterial hypertension, compensated HT and overweight/obesity (median age - 56.0 years, 33 women) completed the main (patients with MDSLD, n=23) and control (patients with an intact liver, n=13) groups. Data processed statistically, presented as median [lower; upper quartile], significance determined by Mann-Whitney, correlations – by Kendall; significance threshold – p<0.05. Results and their discussion. In 23 patients with hypothyroidism and hypertension, endocrine MDSLD was present, which was manifested by a significant increase in the right lobe of the liver and the diameter of the portal vein, greater morpho-functional characteristics of obesity, a worse thyroid-hormonal profile, and hyperleptinemia in 19 people. Conclusions. In addition to diabetes mellitus and obesity, MDSLD is often associated with HT, polycystic ovary syndrome, hypogonadism and growth hormone deficiency when it occurs by hormone-dependent mechanisms and quickly progresses, worsening the course of endocrine pathology. In patients with HT, MDSLD was accompanied by worse characteristics of obesity, and thyroid hormone profile, as well as hyperleptinemia.
References
2. Lonardo A, Carani C, Carulli N, Loria P. 'Endocrine NAFLD' a hormonocentric perspective of nonalcoholic fatty liver disease pathogenesis. J Hepatol. 2006 Jun;44(6):1196-207. doi: 10.1016/j.jhep.2006.03.005.
3. Quek J, Chan KE, Wong ZY, Tan C, Tan B, Lim WH, et al. Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2023 Jan;8(1):20-30. doi: 10.1016/S2468-1253(22)00317-X.
4. Xie J, Huang H, Liu Z, Li Y, Yu C, Xu L, et al. The associations between modifiable risk factors and nonalcoholic fatty liver disease: A comprehensive Mendelian randomization study. Hepatology. 2023 Mar 1;77(3):949-64. doi: 10.1002/hep.32728.
5. Lonardo A, Mantovani A, Lugari S, Targher G. NAFLD in some common endocrine diseases: prevalence, pathophysiology, and principles of diagnosis and management. Int J Mol Sci. 2019 Jun 11;20(11):2841. doi: 10.3390/ijms20112841.
6. Shen M, Shi H. Sex hormones and their receptors regulate liver energy homeostasis. Int J Endocrinol. 2015;2015:294278. doi: 10.1155/2015/294278.
7. Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004 Jan;19(1):41-7. doi: 10.1093/humrep/deh098.
8. Targher G, Rossini M, Lonardo A. Evidence that non-alcoholic fatty liver disease and polycystic ovary syndrome are associated by necessity rather than chance: a novel hepato-ovarian axis? Endocrine. 2016 Feb;51(2):211-21. doi: 10.1007/s12020-015-0640-8.
9. Wu J, Yao XY, Shi RX, Liu SF, Wang XY. A potential link between polycystic ovary syndrome and non-alcoholic fatty liver disease: an update meta-analysis. Reprod Health. 2018 May 10;15(1):77. doi: 10.1186/s12978-018-0519-2.
10. Munir I, Yen HW, Geller DH, Torbati D, Bierden RM, Weitsman SR, et al. Insulin augmentation of 17alpha-hydroxylase activity is mediated by phosphatidyl inositol 3-kinase but not extracellular signal-regulated kinase-1/2 in human ovarian theca cells. Endocrinology. 2004 Jan;145(1):175-83. doi: 10.1210/en.2003-0329.
11. Abbott DH, Dumesic DA, Levine JE. Hyperandrogenic origins of polycystic ovary syndrome - implications for pathophysiology and therapy. Expert Rev Endocrinol Metab. 2019 Mar;14(2):131-43. doi: 10.1080/17446651.2019.1576522.
12. Schiffer L, Kempegowda P, Arlt W, O'Reilly MW. Mechanisms in endocrinology: the sexually dimorphic role of androgens in human metabolic disease. Eur J Endocrinol. 2017 Sep;177(3):R125-43. doi: 10.1530/EJE-17-0124.
13. Kander MC, Cui Y, Liu Z. Gender difference in oxidative stress: a new look at the mechanisms for cardiovascular diseases. J Cell Mol Med. 2017 May;21(5):1024-32. doi: 10.1111/jcmm.13038.
14. Liu C, Schönke M, Spoorenberg B, Lambooij JM, van der Zande HJP, Zhou E, et al. FGF21 protects against hepatic lipotoxicity and macrophage activation to attenuate fibrogenesis in nonalcoholic steatohepatitis. Elife. 2023 Jan 17;12:e83075. doi: 10.7554/eLife.83075.
15. Harada N, Hanaoka R, Hanada K, Izawa T, Inui H, Yamaji R. Hypogonadism alters cecal and fecal microbiota in male mice. Gut Microbes. 2016 Nov;7(6):533-9. doi: 10.1080/19490976.2016.1239680.