加拿大阿尔伯塔大学的理查德·雷勒及其带领的研究小组找到了降低血液中脂肪含量的新方法，通过抑制一种被称为甘油三酯水解酶（TGH）的活性，可降低动物血脂含量，并改善葡萄糖的新陈代谢。
在加拿大，有60%的人身体超重甚至肥胖，肥胖症已经成为广受关注的疾病。肥胖症引发的主要问题之一是血液中的脂肪水平增高，这又是导致心血管病和脂肪肝以及Ⅱ型糖尿病的主要原因。
在动物身上的实验还表明，使用这种方法可以防止脂肪在肝脏等器官中的堆积，避免脂肪肝的形成。同时，降低TGH酶的活性还可以保护胰腺中的β细胞，而胰腺正是身体生产胰岛素的关键器官，因此该方法有助于减少肥胖病患者患糖尿病的风险。
研究人员表示，该项发现表明TGH酶最终可以成为药物标靶，用于治疗肥胖症引发的代谢并发症，有助于人们预防这些与肥胖症相关的疾病。研究成果发表在3月份出版的《细胞代谢》杂志上。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell Metabolism, Volume 11, Issue 3, 183-193, 3 March 2010 10.1016/j.cmet.2010.02.005
Loss of TGH/Ces3 in Mice Decreases Blood Lipids, Improves Glucose Tolerance, and Increases Energy Expenditure
Enhui Wei, Yassine Ben Ali, James Lyon, Huajin Wang, Randy Nelson, Vernon W. Dolinsky, Jason R.B. Dyck, Grant Mitchell, Gregory S. Korbutt, Richard Lehner
Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2S2, Canada Department of Cell Biology, University of Alberta, Edmonton, AB T6G 2S2, Canada Group on Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, AB T6G 2S2, Canada Department of Surgery, University of Alberta, Edmonton, AB T6G 2E1, Canada Department of Pediatrics, CHU Sainte-Justine, Université de Montreal, Montreal, QC H3T 1C5, Canada Corresponding author
Excessive accumulation of triacylglycerol in peripheral tissues is tightly associated with obesity and has been identified as an independent risk factor for insulin resistance, type 2 diabetes, and cardiovascular complications. Here we show that ablation of carboxylesterase 3 (Ces3)/triacylglycerol hydrolase (TGH) expression in mice (Tgh−/− ) results in decreased plasma triacylglycerol, apolipoprotein B, and fatty acid levels in both fasted and fed states. Despite the attenuation of very low-density lipoprotein secretion, TGH deficiency does not increase hepatic triacylglycerol levels. Tgh−/− mice exhibit increased food intake, respiratory quotient, and energy expenditure without change in body weight. These metabolic changes are accompanied by improved insulin sensitivity and glucose tolerance. Tgh−/− mice have smaller sized pancreatic islets but maintain normal glucose-stimulated insulin secretion. These studies demonstrate the potential of TGH as a therapeutic target for lowering blood lipid levels.
