多囊卵巢综合征合并非酒精性脂肪性肝病的危险因素

王东旭; 邢川; 吕波; 赵涵; 何冰

doi:10.3969/j.issn.1001-5256.2021.10.046

多囊卵巢综合征合并非酒精性脂肪性肝病的危险因素

DOI: 10.3969/j.issn.1001-5256.2021.10.046

王东旭^1a,
邢川^1b,
吕波²,
赵涵^1b,
何冰^1b, ,

1a.
中国医科大学附属盛京医院消化内科，沈阳 110004
1b.
中国医科大学附属盛京医院内分泌科, 沈阳 110004
2.
大连市第三人民医院内分泌科，辽宁大连 116033

基金项目:

国家自然科学基金 (81570765)

详细信息

通信作者:
何冰，hebing7557@163.com

中图分类号: R575.5
计量
- 文章访问数: 529
- HTML全文浏览量: 216
- PDF下载量: 41
- 被引次数: 0
出版历程
- 收稿日期: 2021-02-04
- 录用日期: 2021-02-20
- 出版日期: 2021-10-20

Risk factors for polycystic ovary syndrome with nonalcoholic fatty liver disease

Dongxu WANG^1a,
Chuan XING^1b,
Bo LYU²,
Han ZHAO^1b,
Bing HE^{1b
, ,}

1a.
Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang 110004, China
1b.
Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang 110004, China
2.
Department of Endocrinology, The Third People's Hospital of Dalian, Dalian, Liaoning 116033, China

Research funding:

National Natural Science Foundation of China (81570765)

摘要

摘要: 多囊卵巢综合征(PCOS)可表现为生殖、内分泌、代谢等多种紊乱, 其中非酒精性脂肪性肝病(NAFLD)的患病率在PCOS人群中显著增高, 目前对于PCOS合并NAFLD的危险因素未完全阐明。从高雄激素血症、胰岛素抵抗、肥胖、血脂异常、慢性低度炎症及肠道菌群失调等方面介绍了PCOS合并NAFLD的研究进展, 为提高对PCOS合并NAFLD的重视与管理提供思路与方法。
- 非酒精性脂肪性肝病 /
- 多囊卵巢综合征 /
- 危险因素
Abstract: Polycystic ovary syndrome (PCOS) manifests as a series of disorders in reproductive system, endocrine, and metabolism, and there is a significant increase in the prevalence rate of nonalcoholic fatty liver disease (NAFLD) in the population with PCOS. At present, the risk factors for PCOS with NAFLD have not been fully clarified. This article introduces the research advances in PCOS with NAFLD from the aspects of hyperandrogenism, insulin resistance, obesity, dyslipidemia, chronic low-grade inflammation, and intestinal flora imbalance, so as to provide ideas and methods for improving the awareness and management of PCOS with NAFLD.
- Non-Alcoholic Fatty Liver Disease /
- Polycystic Ovary Syndrome /
- Risk Factors

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参考文献(42)

[1]	ROCHA AL, OLIVEIRA FR, AZEVEDO RC, et al. Recent advances in the understanding and management of polycystic ovary syndrome[J]. F1000Res, 2019, 8: F1000 Faculty Rev-565. DOI: 10.12688/f1000research.15318.1.
[2]	CONWAY G, DEWAILLY D, DIAMANTI-KANDARAKIS E, et al. The polycystic ovary syndrome: A position statement from the European Society of Endocrinology[J]. Eur J Endocrinol, 2014, 171(4): p1-p29. DOI: 10.1530/EJE-14-0253.
[3]	WANG J, WU D, GUO H, et al. Hyperandrogenemia and insulin resistance: The chief culprit of polycystic ovary syndrome[J]. Life Sci, 2019, 236: 116940. DOI: 10.1016/j.lfs.2019.116940.
[4]	ZENG X, XIE YJ, LIU YT, et al. Polycystic ovarian syndrome: Correlation between hyperandrogenism, insulin resistance and obesity[J]. Clin Chim Acta, 2020, 502: 214-221. DOI: 10.1016/j.cca.2019.11.003.
[5]	IGNATOV A, ORTMANN O. Endocrine risk factors of endometrial cancer: Polycystic ovary syndrome, oral contraceptives, infertility, tamoxifen[J]. Cancers (Basel), 2020, 12(7): 1766. DOI: 10.3390/cancers12071766.
[6]	SUNAMI Y. NASH, Fibrosis and hepatocellular carcinoma: Lipid synthesis and glutamine/acetate signaling[J]. Int J Mol Sci, 2020, 21(18): 6799. DOI: 10.3390/ijms21186799.
[7]	PAFILI K, RODEN M. Nonalcoholic fatty liver disease (NAFLD) from pathogenesis to treatment concepts in humans[J]. Mol Metab, 2021, 50: 101122. DOI: 10.1016/j.molmet.2020.101122.
[8]	SALVA-PASTOR N, LÓPEZ-SÁNCHEZ GN, CHÁVEZ-TAPIA NC, et al. Polycystic ovary syndrome with feasible equivalence to overweight as a risk factor for non-alcoholic fatty liver disease development and severity in Mexican population[J]. Ann Hepatol, 2020, 19(3): 251-257. DOI: 10.1016/j.aohep.2020.01.004.
[9]	ZHANG J, HU J, ZHANG C, et al. Analyses of risk factors for polycystic ovary syndrome complicated with non-alcoholic fatty liver disease[J]. Exp Ther Med, 2018, 15(5): 4259-4264. DOI: 10.3892/etm.2018.5932.
[10]	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.
[11]	QIAN ZW, YAO Q, ZHOU G, et al. Advances in neuroendocrine mechanism of polycystic ovary syndrome[J]. J Int Reprod Health/Fam Plan, 2021, 40(1): 79-83. DOI: 10.12280/gjszjk.20200249. 钱紫薇, 姚琦, 周阁, 等. 多囊卵巢综合征神经内分泌病因机制的研究进展[J]. 国际生殖健康/计划生育杂志, 2021, 40(1): 79-83. DOI: 10.12280/gjszjk.20200249
[12]	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.
[13]	BARANOVA A, TRAN TP, AFENDY A, et al. Molecular signature of adipose tissue in patients with both non-alcoholic fatty liver disease (NAFLD) and polycystic ovarian syndrome (PCOS)[J]. J Transl Med, 2013, 11: 133. DOI: 10.1186/1479-5876-11-133.
[14]	SAEZ-LOPEZ C, BARBOSA-DESONGLES A, HERNANDEZ C, et al. Sex hormone-binding globulin reduction in metabolic disorders may play a role in NAFLD development[J]. Endocrinology, 2017, 158(3): 545-559. DOI: 10.1210/en.2016-1668.
[15]	ZHANG Y, MENG F, SUN X, et al. Hyperandrogenism and insulin resistance contribute to hepatic steatosis and inflammation in female rat liver[J]. Oncotarget, 2018, 9(26): 18180-18197. DOI: 10.18632/oncotarget.24477.
[16]	CONDORELLI RA, CALOGERO AE, DI MAURO M, et al. Androgen excess and metabolic disorders in women with PCOS: Beyond the body mass index[J]. J Endocrinol Invest, 2018, 41(4): 383-388. DOI: 10.1007/s40618-017-0762-3.
[17]	WELT CK, DURAN JM. Genetics of polycystic ovary syndrome[J]. Semin Reprod Med, 2014, 32(3): 177-182. DOI: 10.1055/s-0034-1371089.
[18]	LU CY, QIAN Y. Mechanisms and drug therapy of insulin resistance in polycystic ovary syndrome[J]. Medical Recapitulate, 2020, 26(22): 4504-4509, 4514. DOI: 10.3969/j.issn.1006-2084.2020.22.026. 陆超亦, 钱云. 多囊卵巢综合征胰岛素抵抗机制与药物治疗[J]. 医学综述, 2020, 26(22): 4504-4509, 4514. DOI: 10.3969/j.issn.1006-2084.2020.22.026.
[19]	HARSHA VARMA S, TIRUPATI S, PRADEEP T, et al. Insulin resistance and hyperandrogenemia independently predict nonalcoholic fatty liver disease in women with polycystic ovary syndrome[J]. Diabetes Metab Syndr, 2019, 13(2): 1065-1069. DOI: 10.1016/j.dsx.2018.12.020.
[20]	BUZZETTI E, PINZANI M, TSOCHATZIS EA. The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD)[J]. Metabolism, 2016, 65(8): 1038-1048. DOI: 10.1016/j.metabol.2015.12.012.
[21]	HIGUCHI N, KATO M, TANAKA M, et al. Effects of insulin resistance and hepatic lipid accumulation on hepatic mRNA expression levels of apoB, MTP and L-FABP in non-alcoholic fatty liver disease[J]. Exp Ther Med, 2011, 2(6): 1077-1081. DOI: 10.3892/etm.2011.328.
[22]	CHATTERJEE A, BASU A, DAS K, et al. Hepatic transcriptome signature correlated with HOMA-IR explains early nonalcoholic fatty liver disease pathogenesis[J]. Ann Hepatol, 2020, 19(5): 472-481. DOI: 10.1016/j.aohep.2020.06.009.
[23]	FURUHASHI M, SAITOH S, SHIMAMOTO K, et al. Fatty acid-binding protein 4 (FABP4): Pathophysiological insights and potent clinical biomarker of metabolic and cardiovascular diseases[J]. Clin Med Insights Cardiol, 2014, 8(Suppl 3): 23-33. DOI: 10.4137/CMC.S17067.
[24]	MOYLAN CA, PANG H, DELLINGER A, et al. Hepatic gene expression profiles differentiate presymptomatic patients with mild versus severe nonalcoholic fatty liver disease[J]. Hepatology, 2014, 59(2): 471-482. DOI: 10.1002/hep.26661.
[25]	XIE LD, ZHANG YN, GONG LF, et al. Pathogenesis of polycystic ovary syndrome with insulin resistance[J]. Matern Child Health Care China, 2019, 34(8): 1926-1929. DOI: 10.7620/zgfybj.j.issn.1001-4411.2019.08.75. 谢来娣, 张伊娜, 龚丽芬, 等. 多囊卵巢综合征伴胰岛素抵抗相关发病机制研究[J]. 中国妇幼保健, 2019, 34(8): 1926-1929. DOI: 10.7620/zgfybj.j.issn.1001-4411.2019.08.75.
[26]	SHENGIR M, KRISHNAMURTHY S, GHALI P, et al. Prevalence and predictors of nonalcoholic fatty liver disease in South Asian women with polycystic ovary syndrome[J]. World J Gastroenterol, 2020, 26(44): 7046-7060. DOI: 10.3748/wjg.v26.i44.7046.
[27]	O'REILLY MW, HOUSE PJ, TOMLINSON JW. Understanding androgen action in adipose tissue[J]. J Steroid Biochem Mol Biol, 2014, 143: 277-284. DOI: 10.1016/j.jsbmb.2014.04.008.
[28]	BARBER TM, HANSON P, WEICKERT MO, et al. Obesity and polycystic ovary syndrome: Implications for pathogenesis and novel management strategies[J]. Clin Med Insights Reprod Health, 2019, 13: 1179558119874042. DOI: 10.1177/1179558119874042.
[29]	HU W, LI L, YANG M, et al. Circulating Sfrp5 is a signature of obesity-related metabolic disorders and is regulated by glucose and liraglutide in humans[J]. J Clin Endocrinol Metab, 2013, 98(1): 290-298. DOI: 10.1210/jc.2012-2466.
[30]	WANG GX, ZHAO XY, MENG ZX, et al. The brown fat-enriched secreted factor Nrg4 preserves metabolic homeostasis through attenuation of hepatic lipogenesis[J]. Nat Med, 2014, 20(12): 1436-1443. DOI: 10.1038/nm.3713.
[31]	CHANG ML, YANG Z, YANG SS. Roles of adipokines in digestive diseases: Markers of inflammation, metabolic alteration and disease progression[J]. Int J Mol Sci, 2020, 21(21). DOI: 10.3390/ijms21218308.
[32]	MAFFAZIOLI G, LOPES CP, HEINRICH-OLIVEIRA V, et al. Prevalence of metabolic disturbances among women with polycystic ovary syndrome in different regions of Brazil[J]. Int J Gynaecol Obstet, 2020, 151(3): 383-391. DOI: 10.1002/ijgo.13374.
[33]	TARANTO D, GUIMARÃES T, COUTO CA, et al. Nonalcoholic fatty liver disease in women with polycystic ovary syndrome: Associated factors and noninvasive fibrosis staging in a single Brazilian center[J]. Arch Endocrinol Metab, 2020, 64(3): 235-242. DOI: 10.20945/2359-3997000000242.
[34]	MARÍ M, CABALLERO F, COLELL A, et al. Mitochondrial free cholesterol loading sensitizes to TNF- and Fas-mediated steatohepatitis[J]. Cell Metab, 2006, 4(3): 185-198. DOI: 10.1016/j.cmet.2006.07.006.
[35]	IOANNOU GN, SUBRAMANIAN S, CHAIT A, et al. Cholesterol crystallization within hepatocyte lipid droplets and its role in murine NASH[J]. J Lipid Res, 2017, 58(6): 1067-1079. DOI: 10.1194/jlr.M072454.
[36]	TOMITA K, TERATANI T, SUZUKI T, et al. Acyl-CoA: Cholesterol acyltransferase 1 mediates liver fibrosis by regulating free cholesterol accumulation in hepatic stellate cells[J]. J Hepatol, 2014, 61(1): 98-106. DOI: 10.1016/j.jhep.2014.03.018.
[37]	RUDNICKA E, KUNICKI M, SUCHTA K, et al. Inflammatory markers in women with polycystic ovary syndrome[J]. Biomed Res Int, 2020, 2020: 4092470. DOI: 10.1155/2020/4092470.
[38]	SPRITZER PM, LECKE SB, SATLER F, et al. Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome[J]. Reproduction, 2015, 149(5): r219-r227. DOI: 10.1530/REP-14-0435.
[39]	KRISHNAN A, MUTHUSAMI S, PERIYASAMY L, et al. Effect of DHT-induced hyperandrogenism on the pro-inflammatory cytokines in a rat model of polycystic ovary morphology[J]. Medicina (Kaunas), 2020, 56(3): 100. DOI: 10.3390/medicina56030100.
[40]	GARCIA-BELTRAN C, MALPIQUE R, CARBONETTO B, et al. Gut microbiota in adolescent girls with polycystic ovary syndrome: Effects of randomized treatments[J]. Pediatr Obes, 2021, 16(4): e12734. DOI: 10.1111/ijpo.12734.
[41]	CHU W, HAN Q, XU J, et al. Metagenomic analysis identified microbiome alterations and pathological association between intestinal microbiota and polycystic ovary syndrome[J]. Fertil Steril, 2020, 113(6): 1286-1298. e4. DOI: 10.1016/j.fertnstert.2020.01.027.
[42]	ZHOU L, NI Z, YU J, et al. Correlation between fecal metabolomics and gut microbiota in obesity and polycystic ovary syndrome[J]. Front Endocrinol (Lausanne), 2020, 11: 628. DOI: 10.3389/fendo.2020.00628.