Menopausal stages and non-alcoholic fatty liver disease in middle-aged women

Ryu, Seungho; Suh, Byung-Seong; Chang, Yoosoo; Kwon, Min-Jung; Yun, Kyung Eun; Jung, Hyun Suk; Kim, Chan-Won; Kim, Bo-Kyoung; Kim, YooJin; Choi, Yuni; Ahn, Jiin; Cho, Yong Soo; Kim, Kyehyun; Ahn, Younjhin; Park, Hyun Young; Chung, Eun Chul; Shin, Hocheol; Cho, Juhee

doi:10.1016/j.ejogrb.2015.04.017

Cited by 40 publications

(34 citation statements)

References 44 publications

(62 reference statements)

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“…Both human and rodent studies provide evidence for a protective effect of estrogen and testosterone on the development of fatty liver (15)(16)(17)(19)(20)(21). We set out to investigate the effect of gonadectomy in three different strains of both sexes.…”

Section: Discussionmentioning

confidence: 99%

“…NASH has been reported to be more prevalent in females than in males (11), and lean women appear to have a higher prevalence of NAFLD than lean men (14). Also, NAFLD has been shown to be more prevalent in post-as compared with premenopausal women, suggesting that sex hormones may influence the onset of NAFLD (15). The fact that breast cancer patients treated with an estrogen receptor antagonist develop massive hepatic steatosis and even typical NASH indicates that estrogen affects development of this disease (16).…”

Section: Accession Numbersmentioning

confidence: 99%

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Genetic and hormonal control of hepatic steatosis in female and male mice

Norheim

Hui

Kulahcioglu

et al. 2017

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Section: Accession Numbersmentioning

confidence: 99%

Genetic and hormonal control of hepatic steatosis in female and male mice

Norheim

Hui

Kulahcioglu

et al. 2017

Journal of Lipid Research

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“…In addition to and independent of the role of MetS and its components, menopausal status [49, 83, 85] and increasing age [49, 56, 82] have all been consistently identified as strong risk factors for NAFLD in women. Only in a few studies was the association between menopausal status and NAFLD no longer significant after adjustment for age and metabolic factors [37, 81], indicating that menopause predisposes to developing NAFLD via incident dysmetabolic traits which typically appear in the postmenopausal age.…”

Section: Epidemiology Of Nafldmentioning

confidence: 99%

NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk

et al. 2017

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Nonalcoholic fatty liver disease (NAFLD) spans steatosis through nonalcoholic steatohepatis, cirrhosis, and hepatocellular carcinoma (HCC) associated with striking systemic features and excess cardiovascular and liver-related mortality. The pathogenesis of NAFLD is complex and multifactorial. Endocrine derangements are closely linked with dysmetabolic traits. For example, in animal and human studies, female sex is protected from dysmetabolism thanks to young individuals’ ability to partition fatty acids towards ketone body production rather than very low density lipoprotein (VLDL)-triacylglycerol, and to sex-specific browning of white adipose tissue. Ovarian senescence facilitates both the development of massive hepatic steatosis and the fibrotic progression of liver disease in an experimental overfed zebrafish model. Consistently, estrogen deficiency, by potentiating hepatic inflammatory changes, hastens the progression of disease in a dietary model of nonalcoholic steatohepatitis (NASH) developing in ovariectomized mice fed a high-fat diet. In humans, NAFLD more often affects men; and premenopausal women are equally protected from developing NAFLD as they are from cardiovascular disease. It would be expected that early menarche, definitely associated with estrogen activation, would produce protection against the risk of NAFLD. Nevertheless, it has been suggested that early menarche may confer an increased risk of NAFLD in adulthood, excess adiposity being the primary culprit of this association. Fertile age may be associated with more severe hepatocyte injury and inflammation, but also with a decreased risk of liver fibrosis compared to men and postmenopausal status. Later in life, ovarian senescence is strongly associated with severe steatosis and fibrosing NASH, which may occur in postmenopausal women. Estrogen deficiency is deemed to be responsible for these findings via the development of postmenopausal metabolic syndrome. Estrogen supplementation may at least theoretically protect from NAFLD development and progression, as suggested by some studies exploring the effect of hormonal replacement therapy on postmenopausal women, but the variable impact of different sex hormones in NAFLD (i.e., the pro-inflammatory effect of progesterone) should be carefully considered.

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“…One side effect of TMX is the development of nonalcoholic fatty liver disease and steatohepatitis (Nishino et al 2003; Murata et al 2000; Oien et al 1999). As women transition to menopause, the risk of non-alcoholic fatty liver disease increases (Ryu et al 2015; Yang et al 2014). Aging is a natural risk factor for NAFLD, which may confound the impact of menopause on risk of NAFLD.…”

Section: Lack Of Estrogen Signaling Promotes Liver Tg Accumulation Anmentioning

confidence: 99%

Role of Estrogens in the Regulation of Liver Lipid Metabolism

Palmisano

Zhu

Stafford

2017

Sex and Gender Factors Affecting Metabolic Homeostasis, Diabetes and Obesity

210

147

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Before menopause, women are protected from atherosclerotic heart disease associated with obesity relative to men. Sex hormones have been proposed as a mechanism that differentiates this risk. In this review, we discuss the literature around how the endogenous sex hormones and hormone treatment approaches after menopause regulate fatty acid, triglyceride and cholesterol metabolism to influence cardiovascular risk. The important regulatory functions of estrogen signaling pathways with regard to lipid metabolism have been in part obscured by clinical trials with hormone treatment of women after menopause, due to different formulations, routes of delivery, and pairings with progestins. Oral hormone treatment with several estrogen preparations increase VLDL triglyceride production. Progestins oppose this effect by stimulating VLDL clearance in both humans and animals. Transdermal estradiol preparations do not increase VLDL production or serum triglycerides. Many aspects of sex-differences in atherosclerotic heart disease risk are influenced by the distributed actions of estrogens in muscle, adipose and liver. In humans, 17β estradiol (E2) is the predominant circulating estrogen, and signals through Estrogen Receptor alpha (ERα), Estrogen Receptor beta (ER β) and G-protein coupled Estrogen Receptor (GPER). Over 1000 human liver genes display a sex-bias in their expression, and the top biological pathways are in lipid metabolism and genes related to cardiovascular disease. Many of these genes display variation depending on estrus cycling in the mouse. Future directions will likely rely on targeting estrogens to specific tissues, or specific aspects of the signaling pathways in order to recapitulate the protective physiology of pre-menopause therapeutically after menopause.

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Menopausal stages and non-alcoholic fatty liver disease in middle-aged women

Cited by 40 publications

References 44 publications

Genetic and hormonal control of hepatic steatosis in female and male mice

Genetic and hormonal control of hepatic steatosis in female and male mice

NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk

Role of Estrogens in the Regulation of Liver Lipid Metabolism

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