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Review
. 2023 Jun 29;5(10):100835.
doi: 10.1016/j.jhepr.2023.100835. eCollection 2023 Oct.

Non-alcoholic fatty liver disease in women - Current knowledge and emerging concepts

Pei Chia Eng  1   2 , Roberta Forlano  1   3 , Tricia Tan  1   2 , Pinelopi Manousou  1   3 , Waljit S Dhillo  1   2 , Chioma Izzi-Engbeaya  1   2
Affiliations
Review

Non-alcoholic fatty liver disease in women - Current knowledge and emerging concepts

Pei Chia Eng et al. JHEP Rep. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease worldwide, affecting up to 30% of adults. Progression to non-alcoholic steatohepatitis (NASH) is a key risk factor for cirrhosis, hepatocellular carcinoma and cardiovascular events. Alterations in reproductive hormones are linked to the development and/or progression of NAFLD/NASH in women. Women with polycystic ovary syndrome and those with oestrogen deficiency are at increased risk of NAFLD/NASH, with higher mortality rates in older women compared to men of similar ages. NAFLD/NASH is currently the leading indication for liver transplantation in women without hepatocellular carcinoma. Therefore, a better understanding of NAFLD in women is needed to improve outcomes. In this review, we discuss the hormonal and non-hormonal factors that contribute to NAFLD development and progression in women. Furthermore, we highlight areas of focus for clinical practice and for future research.

Keywords: Androgens; Estrogens; Menopause; Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Women.

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Conflict of interest statement

All authors report no potential conflicts of interest. Please refer to the accompanying ICMJE disclosure forms for further details.

Figures

Fig. 1
Fig. 1
Changes occur in adipose tissue, liver and skeletal muscle during the menopause that have detrimental metabolic effects. These may contribute to the increased prevalence of metabolic conditions in post-menopausal women.
Fig. 2
Fig. 2
Interactions between adipose tissue, muscle and liver contribute to the development and progression of NAFLD in women. Adipokines and myokines (such as myostatin) mediate adipose tissue-muscle interactions. Ageing and the menopause (i.e. oestrogen deficiency) increase VAT depots and reduce muscle mass and quality. Expanded VAT depots increase FFA delivery to the liver, which has detrimental effects. These alterations in body composition contribute to insulin resistance, hyperglycaemia and/or hyperlipidaemia, with consequent development and progression of NAFLD. FFA, free fatty acid; NAFLD, non-alcoholic fatty liver disease; VAT, visceral adipose tissue.
Fig. 3
Fig. 3
Women with certain conditions (PCOS and Turner syndrome) are at an increased risk of NASH and cirrhosis. In addition, pre-menopausal women are less likely to have resolution of NASH following weight loss. Post-menopausal women have increased prevalence of NAFLD, increased risk of NASH progression and death (due to CVD and liver failure requiring OLT). There are several unmet needs in clinical practice, which if addressed, may improve outcomes. CVD, cardiovascular disease; NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; PCOS, polycystic ovary syndrome; OLT, orthotopic liver transplantation.
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