Fatty acid oxidation is decreased in the liver of ovariectomized rats.

Estrogen-deficient states are associated with hepatic steatosis. Based on previous findings obtained at the molecular and enzymatic levels, it has been suggested that estradiol exerts its lipid-lowering effects in liver through partitioning of triacylglycerols into oxidative pathways. However, information on relevant physiological response was lacking. Therefore, the purpose of the present study was to assess fatty acid oxidation rate in the liver of intact and ovariectomized rats. Tritiated water released from liver slices incubated with 9,10-[ (3)H]palmitate was measured as a reflection of in vivo fatty acid metabolism. Fatty acid oxidation rate was lowered by 34% (p<0.05), associated with 114% higher (p<0.01) hepatic triacylgylcerol content in the liver of ovariectomized as compared to intact rats. Estrogen replacement prevented all of these changes. Fatty liver has been linked with hepatic leptin resistance in obese male rats. Since leptin stimulates fatty acid oxidation in liver, we hypothesized that increased liver triacylglycerol content and decreased fatty acid oxidation might be associated with leptin resistance in ovariectomized rats. To this end, acute leptin delivery was performed. The 120-min intravenous leptin infusion increases fatty acid oxidation by 23% in the liver of ovariectomized rats, which was coupled with 24% lower hepatic triacylglycerol content. We conclude that fatty acid oxidation is decreased in the liver of ovariectomized rats, which is likely to contribute to hepatic steatosis development. Furthermore, our results suggest that leptin sensitivity is not completely lost in the liver of rats ovariectomized for 5 weeks.