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    脂肪肝容易造成肥胖或者二型糖尿病，進一步將發展成肝硬化和肝癌。目前的藥物治療缺乏確鑿的療效，因此治療選擇是有限的。新的研究證實可以從抑制肝臟脂肪合成或肝臟炎癥入手開發治療。

    美國斯克利普斯研究院教授Thomas Burris帶領的團隊致力于研究一類對脂肪產生有重要作用的蛋白LXR，LXR的一種反向激動劑SR9238通過抑制其功能來抑制肝臟脂肪的產生，從而有效緩解和治愈脂肪肝。由于SR9238在肝中能夠迅速的分解，從而不能進入血液，所以SR9238沒有其他副作用。

    研究人員用小鼠做模型研究SR9238的治療效果。他們發現經過一個月的治療，高脂小鼠的肝臟中產生脂肪的基因被抑制，肝臟中脂肪減少達90%。同時他們發現產生膽固醇的酶減少達80%，肝臟損傷標記物同樣有所減少。研究人員發現SR9238對酒精肝同樣有一定的治療效果。

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.