国际生殖健康/计划生育 ›› 2021, Vol. 40 ›› Issue (4): 328-333.doi: 10.12280/gjszjk.20210022
收稿日期:
2021-01-14
出版日期:
2021-07-15
发布日期:
2021-07-27
通讯作者:
谢青贞
E-mail:2528433868@qq.com
基金资助:
PENG Yang-yang, XIE Qing-zhen△()
Received:
2021-01-14
Published:
2021-07-15
Online:
2021-07-27
Contact:
XIE Qing-zhen
E-mail:2528433868@qq.com
摘要:
多囊卵巢综合征(polycystic ovary syndrome,PCOS)是育龄期妇女常见的生殖内分泌紊乱性疾病,且常伴肥胖、胰岛素抵抗(insulin resistance,IR)和脂代谢紊乱等代谢异常。非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)是常见的慢性非酒精性肝脏疾病,包括非酒精性单纯性脂肪肝病、非酒精性脂肪性肝炎、肝纤维化、肝硬化及肝细胞癌等一系列肝脏病变。近年来研究发现PCOS中NAFLD的发病率增加,且两者经常共存,越来越多的研究提出PCOS重要的病理生理机制之一高雄激素血症(hyperandrogenemia,HA)在PCOS相关NAFLD发病机制中发挥重要作用。
彭洋洋, 谢青贞. 雄激素在多囊卵巢综合征合并非酒精性脂肪性肝病中的研究进展[J]. 国际生殖健康/计划生育, 2021, 40(4): 328-333.
PENG Yang-yang, XIE Qing-zhen. Research Progress of Androgen in Polycystic Ovary Syndrome with Non-Alcoholic Fatty Liver Disease[J]. Journal of International Reproductive Health/Family Planning, 2021, 40(4): 328-333.
[1] |
Teede HJ, Misso ML, Costello MF, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome[J]. Hum Reprod, 2018, 33(9):1602-1618. doi: 10.1093/humrep/dey256.
doi: 10.1093/humrep/dey256 URL |
[2] |
Chen Z, Yu Y, Cai J, et al. Emerging Molecular Targets for Treatment of Nonalcoholic Fatty Liver Disease[J]. Trends Endocrinol Metab, 2019, 30(12):903-914. doi: 10.1016/j.tem.2019.08.006.
doi: 10.1016/j.tem.2019.08.006 URL |
[3] |
Asfari MM, Sarmini MT, Baidoun F, et al. Association of non-alcoholic fatty liver disease and polycystic ovarian syndrome[J]. BMJ Open Gastroenterol, 2020, 7(1):e000352. doi: 10.1136/bmjgast-2019-000352.
doi: 10.1136/bmjgast-2019-000352 URL |
[4] |
Brown AJ, Tendler DA, McMurray RG, et al. Polycystic ovary syndrome and severe nonalcoholic steatohepatitis: beneficial effect of modest weight loss and exercise on liver biopsy findings[J]. Endocr Pract, 2005, 11(5):319-324. doi: 10.4158/EP.11.5.319.
doi: 10.4158/EP.11.5.319 pmid: 16191492 |
[5] |
Paschou SA, Polyzos SA, Anagnostis P, et al. Nonalcoholic fatty liver disease in women with polycystic ovary syndrome[J]. Endocrine, 2020, 67(1):1-8. doi: 10.1007/s12020-019-02085-7.
doi: 10.1007/s12020-019-02085-7 URL |
[6] |
Kim JJ, Kim D, Yim JY, et al. Polycystic ovary syndrome with hyperandrogenism as a risk factor for non-obese non-alcoholic fatty liver disease[J]. Aliment Pharmacol Ther, 2017, 45(11):1403-1412. doi: 10.1111/apt.14058.
doi: 10.1111/apt.14058 URL |
[7] |
Wu J, Yao XY, Shi RX, et al. A potential link between polycystic ovary syndrome and non-alcoholic fatty liver disease: an update meta-analysis[J]. Reprod Health, 2018, 15(1):77. doi: 10.1186/s12978-018-0519-2.
doi: 10.1186/s12978-018-0519-2 URL |
[8] |
Wang X, Li Q, Pang J, et al. Associations between serum total, free and bioavailable testosterone and non-alcoholic fatty liver disease in community-dwelling middle-aged and elderly women[J]. Diabetes Metab, 2021, 47(3):101199. doi: 10.1016/j.diabet.2020. 09.007.
doi: 10.1016/j.diabet.2020. 09.007 URL |
[9] |
Qu X, Donnelly R. Sex Hormone-Binding Globulin (SHBG) as an Early Biomarker and Therapeutic Target in Polycystic Ovary Syndrome[J]. Int J Mol Sci, 2020, 21(21):8191. doi: 10.3390/ijms21218191.
doi: 10.3390/ijms21218191 URL |
[10] |
Wang X, Xie J, Pang J, et al. Serum SHBG Is Associated With the Development and Regression of Nonalcoholic Fatty Liver Disease: A Prospective Study[J]. J Clin Endocrinol Metab, 2020, 105(3):dgz244. doi: 10.1210/clinem/dgz244.
doi: 10.1210/clinem/dgz244 |
[11] |
Xiao J, Wang F, Wong NK, et al. Global liver disease burdens and research trends: Analysis from a Chinese perspective[J]. J Hepatol, 2019, 71(1):212-221. doi: 10.1016/j.jhep.2019.03.004.
doi: S0168-8278(19)30140-0 pmid: 30871980 |
[12] |
Risal S, Pei Y, Lu H, et al. Prenatal androgen exposure and transgenerational susceptibility to polycystic ovary syndrome[J]. Nat Med, 2019, 25(12):1894-1904. doi: 10.1038/s41591-019-0666-1.
doi: 10.1038/s41591-019-0666-1 URL |
[13] |
Cheng YW, Chen KW, Kuo HC, et al. Specific diacylglycerols generated by hepatic lipogenesis stimulate the oncogenic androgen receptor activity in male hepatocytes[J]. Int J Obes(Lond), 2019, 43(12):2469-2479. doi: 10.1038/s41366-019-0431-z.
doi: 10.1038/s41366-019-0431-z URL |
[14] |
Li T, Zhang T, Cui T, et al. Involvement of endogenous testosterone in hepatic steatosis in women with polycystic ovarian syndrome[J]. J Steroid Biochem Mol Biol, 2020, 204:105752. doi: 10.1016/j.jsbmb.2020.105752.
doi: 10.1016/j.jsbmb.2020.105752 URL |
[15] |
Abruzzese GA, Heber MF, Ferrer MJ, et al. Effects of in utero androgen excess and metformin treatment on hepatic functions[J]. Mol Cell Endocrinol, 2019, 491:110416. doi: 10.1016/j.mce.2019.03.006.
doi: S0303-7207(19)30082-6 pmid: 30880153 |
[16] |
Hamaguchi M, Kojima T, Ohbora A, et al. Aging is a risk factor of nonalcoholic fatty liver disease in premenopausal women[J]. World J Gastroenterol, 2012, 18(3):237-243. doi: 10.3748/wjg.v18.i3.237.
doi: 10.3748/wjg.v18.i3.237 URL |
[17] |
McKenzie J, Fisher BM, Jaap AJ, et al. Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo-controlled trial[J]. Clin Endocrinol(Oxf), 2006, 65(1):40-44. doi: 10.1111/j.1365-2265.2006.02543.x.
doi: 10.1111/j.1365-2265.2006.02543.x URL |
[18] |
Meda C, Barone M, Mitro N, et al. Hepatic ERα accounts for sex differences in the ability to cope with an excess of dietary lipids[J]. Mol Metab, 2020, 32:97-108. doi: 10.1016/j.molmet.2019.12.009.
doi: 10.1016/j.molmet.2019.12.009 URL |
[19] |
Sarkar M, Terrault N, Chan W, et al. Polycystic ovary syndrome (PCOS) is associated with NASH severity and advanced fibrosis[J]. Liver Int, 2020, 40(2):355-359. doi: 10.1111/liv.14279.
doi: 10.1111/liv.14279 URL |
[20] |
Sarkar MA, Suzuki A, Abdelmalek MF, et al. Testosterone is Associated With Nonalcoholic Steatohepatitis and Fibrosis in Premenopausal Women With NAFLD[J]. Clin Gastroenterol Hepatol, 2021, 19(6):1267-1274. doi: 10.1016/j.cgh.2020.09.045.
doi: 10.1016/j.cgh.2020.09.045 URL |
[21] |
Park JM, Lee HS, Oh J, et al. Serum Testosterone Level Within Normal Range Is Positively Associated with Nonalcoholic Fatty Liver Disease in Premenopausal but Not Postmenopausal Women[J]. J Womens Health(Larchmt), 2019, 28(8):1077-1082. doi: 10.1089/jwh.2018.7263.
doi: 10.1089/jwh.2018.7263 |
[22] |
Qiu X, Wei Y, Liu C, et al. Hyperandrogen enhances apoptosis of human ovarian granulosa cells via up-regulation and demethylation of PDCD4[J]. Gynecol Endocrinol, 2020, 36(4):333-337. doi: 10.1080/09513590.2019.1653844.
doi: 10.1080/09513590.2019.1653844 URL |
[23] |
Azhary J, Harada M, Takahashi N, et al. Endoplasmic Reticulum Stress Activated by Androgen Enhances Apoptosis of Granulosa Cells via Induction of Death Receptor 5 in PCOS[J]. Endocrinology, 2019, 160(1):119-132. doi: 10.1210/en.2018-00675.
doi: 10.1210/en.2018-00675 URL |
[24] |
Kupreeva M, Diane A, Lehner R, et al. Effect of metformin and flutamide on insulin, lipogenic and androgen-estrogen signaling, and cardiometabolic risk in a PCOS-prone metabolic syndrome rodent model[J]. Am J Physiol Endocrinol Metab, 2019, 316(1):E16-E33. doi: 10.1152/ajpendo.00018.2018.
doi: 10.1152/ajpendo.00018.2018 URL |
[25] |
Polyzos SA, Kountouras J, Mantzoros CS, et al. Effects of combined low-dose spironolactone plus vitamin E vs vitamin E monotherapy on insulin resistance, non-invasive indices of steatosis and fibrosis, and adipokine levels in non-alcoholic fatty liver disease: a randomized controlled trial[J]. Diabetes Obes Metab, 2017, 19(12):1805-1809. doi: 10.1111/dom.12989.
doi: 10.1111/dom.12989 URL |
[26] |
Wada T, Kenmochi H, Miyashita Y, et al. Spironolactone improves glucose and lipid metabolism by ameliorating hepatic steatosis and inflammation and suppressing enhanced gluconeogenesis induced by high-fat and high-fructose diet[J]. Endocrinology, 2010, 151(5):2040-2049. doi: 10.1210/en.2009-0869.
doi: 10.1210/en.2009-0869 URL |
[27] |
Olaniyi KS, Oniyide AA, Adeyanju OA, et al. Low dose spironolactone-mediated androgen-adiponectin modulation alleviates endocrine-metabolic disturbances in letrozole-induced PCOS[J]. Toxicol Appl Pharmacol, 2021, 411:115381. doi: 10.1016/j.taap.2020.115381.
doi: 10.1016/j.taap.2020.115381 URL |
[28] |
Sanyal AJ. Past, present and future perspectives in nonalcoholic fatty liver disease[J]. Nat Rev Gastroenterol Hepatol, 2019, 16(6):377-386. doi: 10.1038/s41575-019-0144-8.
doi: 10.1038/s41575-019-0144-8 pmid: 31024089 |
[29] |
Friedman SL, Neuschwander-Tetri BA, Rinella M, et al. Mechanisms of NAFLD development and therapeutic strategies[J]. Nat Med, 2018, 24(7):908-922. doi: 10.1038/s41591-018-0104-9.
doi: 10.1038/s41591-018-0104-9 pmid: 29967350 |
[30] |
Andrisse S, Childress S, Ma Y, et al. Low-Dose Dihydrotestosterone Drives Metabolic Dysfunction via Cytosolic and Nuclear Hepatic Androgen Receptor Mechanisms[J]. Endocrinology, 2017, 158(3):531-544. doi: 10.1210/en.2016-1553.
doi: 10.1210/en.2016-1553 pmid: 27967242 |
[31] |
Rostamtabar M, Esmaeilzadeh S, Tourani M, et al. Pathophysiological roles of chronic low-grade inflammation mediators in polycystic ovary syndrome[J]. J Cell Physiol, 2021, 236(2):824-838. doi: 10.1002/jcp.29912.
doi: 10.1002/jcp.29912 URL |
[32] |
Sarkar M, Wellons M, Cedars MI, et al. Testosterone Levels in Pre-Menopausal Women are Associated With Nonalcoholic Fatty Liver Disease in Midlife[J]. Am J Gastroenterol, 2017, 112(5):755-762. doi: 10.1038/ajg.2017.44.
doi: 10.1038/ajg.2017.44 URL |
[33] |
Cox MJ, Edwards MC, Rodriguez Paris V, et al. Androgen Action in Adipose Tissue and the Brain are Key Mediators in the Development of PCOS Traits in a Mouse Model[J]. Endocrinology, 2020, 161(7):bqaa061. doi: 10.1210/endocr/bqaa061.
doi: 10.1210/endocr/bqaa061 |
[34] |
O′Reilly MW, Kempegowda P, Walsh M, et al. AKR1C3-Mediated Adipose Androgen Generation Drives Lipotoxicity in Women With Polycystic Ovary Syndrome[J]. J Clin Endocrinol Metab, 2017, 102(9):3327-3339. doi: 10.1210/jc.2017-00947.
doi: 10.1210/jc.2017-00947 URL |
[35] |
Traish A, Bolanos J, Nair S, et al. Do Androgens Modulate the Pathophysiological Pathways of Inflammation? Appraising the Contemporary Evidence[J]. J Clin Med, 2018, 7(12):549. doi: 10.3390/jcm7120549.
doi: 10.3390/jcm7120549 URL |
[36] |
Moulana M. Immunophenotypic profile of leukocytes in hyperandrogenemic female rat an animal model of polycystic ovary syndrome[J]. Life Sci, 2019, 220:44-49. doi: 10.1016/j.lfs.2019. 01.048.
doi: 10.1016/j.lfs.2019. 01.048 URL |
[37] |
Kakino S, Ohki T, Nakayama H, et al. Pivotal Role of TNF-α in the Development and Progression of Nonalcoholic Fatty Liver Disease in a Murine Model[J]. Horm Metab Res, 2018, 50(1):80-87. doi: 10.1055/s-0043-118666.
doi: 10.1055/s-0043-118666 URL |
[38] |
Saklamaz A, Calan M, Yilmaz O, et al. Polycystic ovary syndrome is associated with increased osteopontin levels[J]. Eur J Endocrinol, 2016, 174(4):415-423. doi: 10.1530/EJE-15-1074.
doi: 10.1530/EJE-15-1074 pmid: 26701868 |
[39] |
Wang Y, Zhou W, Wu C, et al. Circulating osteopontin and its association with liver fat content in non-obese women with polycystic ovary syndrome: a case control study[J]. Reprod Biol Endocrinol, 2018, 16(1):31. doi: 10.1186/s12958-018-0331-4.
doi: 10.1186/s12958-018-0331-4 URL |
[40] |
Tang M, Jiang Y, Jia H, et al. Osteopontin acts as a negative regulator of autophagy accelerating lipid accumulation during the development of nonalcoholic fatty liver disease[J]. Artif Cells Nanomed Biotechnol, 2020, 48(1):159-168. doi: 10.1080/21691401. 2019.1699822.
doi: 10.1080/21691401.2019.1699822 pmid: 31852298 |
[41] |
Wu J, Wu D, Zhang L, et al. NK cells induce hepatic ER stress to promote insulin resistance in obesity through osteopontin production[J]. J Leukoc Biol, 2020, 107(4):589-596. doi: 10.1002/JLB.3MA1119-173R.
doi: 10.1002/JLB.3MA1119-173R URL |
[42] |
Zhu C, Kim K, Wang X, et al. Hepatocyte Notch activation induces liver fibrosis in nonalcoholic steatohepatitis[J]. Sci Transl Med, 2018, 10(468):eaat0344. doi: 10.1126/scitranslmed.aat0344.
doi: 10.1126/scitranslmed.aat0344 |
[43] |
Arriazu E, Ge X, Leung TM, et al. Signalling via the osteopontin and high mobility group box-1 axis drives the fibrogenic response to liver injury[J]. Gut, 2017, 66(6):1123-1137. doi: 10.1136/gutjnl-2015-310752.
doi: 10.1136/gutjnl-2015-310752 pmid: 26818617 |
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