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Submitted on October 14, 2003
Accepted on December 8, 2003
1 Prince Henry's Institute of Medical Research, P.O. Box 5152, Clayton, Vic 3168, Australia and Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
* To whom correspondence should be addressed. E-mail: Kylie.Hewitt{at}phimr.monash.edu.au.
The aromatase knockout (ArKO) mouse cannot synthesize endogenous estrogens due to a disruption to the Cyp19 gene. Previously, we have shown both male and female ArKO mice have an age progressive obese phenotype, and a sexually dimorphic disruption to hepatic cholesterol and triglyceride homeostasis. Only ArKO males have elevated hepatic triglyceride levels leading to hepatic steatosis partly due to an increase in expression of enzymes involved in de novo lipogenesis and transporters involved in fatty acid uptake. In this study ArKO males were treated with 17
-estradiol (3 µg/ kg/ day) at 18 weeks old for 6 weeks. WT controls were not treated and ArKO controls received vehicle oil injections. Estrogen replacement reverses the previously reported obese and fatty liver phenotypes; this was achieved by reductions in gonadal, visceral and brown adipose tissue weights and significantly decreased hepatic triglyceride levels. Estrogen deficiency led to a significant up-regulation of hepatic fatty acid synthase expression which was reduced with 17-estradiol replacement, although not quite reaching significance. Acetyl CoA carboxylase 
mRNA expression showed no significant changes. Expression of transcripts encoding adipocyte differentiated regulatory protein, a fatty acid transporter, was significantly elevated in estrogen deficient males and 17-estradiol replacement significantly reduced these levels. Scavenger receptor class b type 1 showed no significantly changes. This study reveals that the previously reported disruption to triglyceride homeostasis in estrogen deficient males can be reversed with 17-estradiol treatment, indicating an important role for estrogen in maintaining triglyceride and fatty acid homeostasis in males.
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