德国伯恩大学的科学家发现了一种先前未知的果蝇基因，该基因能够调控脂肪代谢。如果果蝇幼虫中缺乏这种基因，则幼虫会丢失了它们全部的脂肪存储。因此，研究人员叫这种基因为'schlank'。在哺乳动物中也存在一组基因，其在结构上与'schlank'非常相似，这些基因可能在能量代谢方面与'schlank'有着相似的功能。
如果科学家破译了一个基因的功能，那么他们就可以去命名该基因。但是果蝇基因的命名并不是按照传统方式的，基因的名字通常暗示着果蝇变成的样子在单独缺失某种基因的情况下。Schlank基因的命名也是这样的。如果该基因是完整的，那么果蝇幼虫能够建立脂肪存储，它将变肥，而基因schlank变异的幼虫，会变得“苗条”。Michael Hoch教授解释说，在极端的例子中，该基因的缺失甚至能够致死。
研究人员对'schlank'做了进一步检测。根据他们的结果，该基因包含一种结构已知的神经酰胺合酶（ceramide synthase）的功能。该酶是作为一种薄膜的原材料能够将机体的细胞围住。此外schlank也有一个调控功能，能够在促进脂质合成的同时抑制存储在体内的脂肪代谢。
这不仅仅在果蝇中发生，人类同样可以产生神经酰胺合酶。人类中存在一组相关的基因称之为Lass基因。神经酰胺合酶对动物来说是很重要的，相关基因的变异将导致严重的代谢紊乱和身体机能故障。研究表明，老鼠的Lass基因能够部分补偿变异果蝇的schlank缺失。
研究人员表示，现在还没有找到哺乳动物的Lass基因与类脂代谢调控的关联。但是根据与schlank基因的比较，他们认为两者的功能应该是非常相似的。如果被证实将有助于开发新的减肥疗法。（生物谷Bioon.com）
生物谷推荐原始出处：
The EMBO Journal 15 October 2009; doi:10.1038/emboj.2009.305
schlank, a member of the ceramide synthase family controls growth and body fat in Drosophila
Reinhard Bauer1, André Voelzmann1, Bernadette Breiden2, Ute Schepers2, Hany Farwanah2, Ines Hahn1, Franka Eckardt1, Konrad Sandhoff2 and Michael Hoch1
1 LIMES-Institute, Program Unit Development, Genetics & Molecular Physiology, Laboratory for Molecular Developmental Biology, University of Bonn, Bonn, Germany
2 LIMES-Institute, Program Unit Membrane Biology & Lipid Biochemistry, c/o Kekulé Institute of Organic Chemistry and Biochemistry, University of Bonn, Bonn, Germany
Ceramide synthases are highly conserved transmembrane proteins involved in the biosynthesis of sphingolipids, which are essential structural components of eukaryotic membranes and can act as second messengers regulating tissue homeostasis. However, the role of these enzymes in development is poorly understood due to the lack of animal models. We identified schlank as a new Drosophila member of the ceramide synthase family. We demonstrate that schlank is involved in the de novo synthesis of a broad range of ceramides, the key metabolites of sphingolipid biosynthesis. Unexpectedly, schlank mutants also show reduction of storage fat, which is deposited as triacylglyerols in the fat body. We found that schlank can positively regulate fatty acid synthesis by promoting the expression of sterol-responsive element-binding protein (SREBP) and SREBP-target genes. It further prevents lipolysis by downregulating the expression of triacylglycerol lipase. Our results identify schlank as a new regulator of the balance between lipogenesis and lipolysis in Drosophila. Furthermore, our studies of schlank and the mammalian Lass2 family member suggest a novel role for ceramide synthases in regulating body fat metabolism.
