Researchers pursued evidence of whether the interaction between the patatin-like phospholipase domain-containing 3 p.I148M variant and the female sex at the genetic and molecular level explains why premenopausal women remain protected against fatty liver disease, while a rapidly progressive disease ensues in some peri- and postmenopausal women.
By Neha MathurSep 28 2023Reviewed by Danielle Ellis, B.Sc. In a recent article published in Nature Medicine, researchers pursued evidence of whether the interaction between the patatin-like phospholipase domain-containing 3 p.I148M variant and the female sex at the genetic and molecular level explains why premenopausal women remain protected against fatty liver disease while a rapidly progressive disease ensues in some peri- and postmenopausal women.
In premenopausal women, high estrogen levels confer protection against FLD; however, during and after menopause, high E2 levels are lost, increasing the susceptibility to developing FLD. Nonalcoholic FLD , a leading cause of cirrhosis and HCC, also occurs in women more than men, especially older postmenopausal women aged ≥55. Furthermore, studies have shown that modulation of estrogen receptor alpha activity increases the risk of steatohepatitis in vulnerable women.
The researchers used data from 1,861 European ancestry from the Liver Biopsy Cohort , who likely had nonalcoholic steatohepatitis . In addition, they age-stratified female patients to capture their reproductive stage and examine the effect of NASH grade as an FLD hallmark. Lastly, the team used the Liver-Bible-2022 cohort encompassing 1,142 healthy individuals aged 40–65 years to examine the role of genetic factors and other noninvasive NAFLD biomarkers to lay the framework to design precision medicine approaches to prevent cardiometabolic diseases associated with NAFLD.
While women aged <45 years remained protected against steatosis, those aged 45–54 and ≥55 years were not. Consistently, the multiplicative interaction with the female sex was specific for the PNPLA3 p.I148M variant; thus, other gene variants contributing to FLD susceptibility, e.g., TM6SF2 p.E167K, did not contribute to FLD risk even in menopausal women.
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