Nonalcoholic fatty liverdisease (NAFLD) includes a range of liver pathology from isolated fat in theliver, to more serious inflammation with or without liver damaging, identifiedas nonalcoholic steatohepatitis (NASH). Though the pathogenesis of NAFLD/NASHis multifactorial, there is a increasing body of literature emphasising the significantinfluence of testosterone to hepatic steatosis in women. Maximum studies connectingtestosterone and NAFLD are grounded in cohorts of women with polycystic ovarysyndrome (PCOS), an endocrinopathy classically marked by metaboliccomorbidities and high androgen levels, such as testosterone. Women with PCOSare a precise high-risk group for NAFLD, and testosterone has been shownto increase their risk of NAFLD, autonomous of obesity and insulin resistance.

As testosterone encouragesother metabolic derangements in women, it is also connected with NAFLD. Withinpostmenopausal women, administration of synthetic testosterone increasesvisceral adiposity. Testosterone has been further shown to directly regulatelipid metabolism within visceral and subcutaneous adipocytes in women.

Whether testosterone mayrepresent a novel target for NAFLD therapeutics warrants consideration,particularly given the limited therapeutic options for this condition.

Testosterone must beconsidered in future studies of NAFLD, as well as broader research prioritiesaddressing the long-term implications of metabolic disease in women. Androgensshould be further considered in therapeutic studies in women, as testosteronemodulation may have farther reaching metabolic effects on insulin resistance,dyslipidemia, and visceral adiposity with benefits that extend from liverhealth and beyond.

Source: J Womens Health (Larchmt). 2019 Aug 1; 28(8): 1015–1016.