脂肪肝容易造成肥胖或者二型糖尿病，进一步将发展成肝硬化和肝癌。目前的药物治疗缺乏确凿的疗效，因此治疗选择是有限的。新的研究证实可以从抑制肝脏脂肪合成或肝脏炎症入手开发治疗。

    美国斯克利普斯研究院教授Thomas Burris带领的团队致力于研究一类对脂肪产生有重要作用的蛋白LXR，LXR的一种反向激动剂SR9238通过抑制其功能来抑制肝脏脂肪的产生，从而有效缓解和治愈脂肪肝。由于SR9238在肝中能够迅速的分解，从而不能进入血液，所以SR9238没有其他副作用。

    研究人员用小鼠做模型研究SR9238的治疗效果。他们发现经过一个月的治疗，高脂小鼠的肝脏中产生脂肪的基因被抑制，肝脏中脂肪减少达90%。同时他们发现产生胆固醇的酶减少达80%，肝脏损伤标记物同样有所减少。研究人员发现SR9238对酒精肝同样有一定的治疗效果。

附：A Liver Selective LXR Inverse Agonist that Suppresses Hepatic Steatosis

    Kristine Griffett, Laura A. Solt, Bahaa El-Dien M. El-Gendy, Theodore M. Kamenecka, Thomas P. Burris

    Fatty liver, which often accompanies obesity and type 2 diabetes, frequently leads to a much more debilitating hepatic disease including non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. Current pharmacological therapies lack conclusive efficacy and thus treatment options are limited. Novel therapeutics that either suppress hepatic lipogenesis and/or hepatic inflammation may be useful. Here, we describe the development of the first selective synthetic LXR inverse agonist (SR9238) and we demonstrate that this compound effectively suppresses hepatic lipogenesis, inflammation and hepatic lipid accumulation in a mouse model of nonalcoholic hepatosteatosis. SR9238 display high potency for both LXRα and LXRβ (40-200 nM IC50) and was designed to display liver specificity so as to avoid potential side effects due to suppression of LXR in the pe**hery. Unexpectedly, treatment of diet induced obese mice with SR9238 suppressed plasma cholesterol levels. These data indicate that liver selective LXR inverse agonists may hold utility in the treatment of liver disease.