摘要：小鼠中的一项新的研究提示，阻断主导脂肪分解的某种酶的药物也许可保护机体不得恶病质（或称消耗综合症）；该综合症表现为肌肉、脂肪的丧失并伴有体重减轻、疲劳和虚弱。 恶病质常见于癌症末期，它是大约15%的癌症患者的死亡原因。 先前的研究大多聚焦于对肌肉丧失机制的了解；人们对脂肪的丧失机制则所知甚少。 如今，Rudolf Zechner及其同事显示，脂肪甘油三酯脂肪酶（或称ATGL，这是一种分解脂肪细胞中储存的脂质的酶）在产生癌症相关性恶病质中起着关键的作用。 研究人员发现，那些在缺乏ATGL基因的生长着肿瘤的小鼠可受到保护而不会罹患癌症相关性恶病质；它们保留了正常的脂肪质量而且几乎没有丧失肌肉。 这些结果指出，ATGL抑制剂（现在尚未研发出来）可能成为恶病质的一种新的疗法。
生物探索推荐英文原文：
Fat-breakdown enzyme the culprit in wasting disease
Drugs that block an enzyme in charge of fat breakdown may protect patients from cachexia, or wasting syndrome, the loss of muscle, fat and accompanying weight loss, fatigue and weakness, hints a new study in mice. Cachexia is often seen in end-stage cancer and is the cause of death in about 15 percent of cancer patients. Previous studies have mostly focused on understanding the loss of muscle mass; little is known about the loss of the fat. Now, Rudolf Zechner and colleagues show that adipose triglyceride lipase, or ATGL, an enzyme that breaks down stored lipids in fat cells, is critical to the development of cancer-associated cachexia. Tumor-bearing mice made genetically deficient in ATGL were protected from cancer-associated cachexia; they retained a normal fat mass and lost almost no muscle, the researchers found. The results point toward ATGL inhibitors (which have yet to be developed) as a potential new treatment for cachexia.
生物探索推荐英文论文摘要：
Science DOI: 10.1126/science.1198973
Adipose Triglyceride Lipase Contributes to Cancer-Associated Cachexia
ABSTRACT
Cachexia is a multifactorial wasting syndrome most common in patients with cancer that is characterized by the uncontrolled loss of adipose and muscle mass. Here, we show that the inhibition of lipolysis through genetic ablation of adipose triglyceride lipase (Atgl) or hormone-sensitive lipase (Hsl) ameliorates certain features of cancer-associated cachexia (CAC). In wildtype C57BL/6 mice, the injection of Lewis lung carcinoma or B16 melanoma cells causes tumor growth, loss of white adipose tissue (WAT), and a marked reduction of gastrocnemius muscle. In contrast, Atgl-deficient mice with tumors resisted the increased WAT lipolysis, myocyte apoptosis, and proteasomal muscle degradation, and maintained normal adipose and gastrocnemius muscle mass. Hsl-deficient mice with tumors were also protected although to a lesser degree. Thus, functional lipolysis is essential in the pathogenesis of CAC. Pharmacological inhibition of metabolic lipases may help prevent cachexia.
