Journal of the Endocrine Society · 7 authors, 14 centres
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Using an inducible mouse model, the study found that deleting the liver estrogen receptor alpha (ERα) before or after sexual maturity did not change high-fat diet-induced liver fat or mitochondrial function, suggesting liver ERα is not required for female protection against these outcomes.
This preclinical study used an inducible mouse model to investigate if liver-specific estrogen receptor alpha (ERα) knockout (LERKO) affects hepatic steatosis and mitochondrial function, and if timing of deletion (pre- vs. post-sexual maturity) matters. Female mice were studied on a short-term or chronic high-fat diet (HFD). Results showed that LERKO mice, compared to controls, did not differ in body weight, liver fat, or mitochondrial oxygen consumption and hydrogen peroxide emission. The timing of LERKO induction also had no significant effect on these mitochondrial or steatosis outcomes. However, hepatic gene expression profiles were altered by LERKO. Limitations include the potential for compensation by other estrogen receptors and the use of a hepatocyte-specific knockout that may spare other liver cell types. The findings suggest the known sexual dimorphism in hepatic steatosis and mitochondrial function is not dependent on direct hepatic ERα signaling.
