很多人为保持身材苗条而不得不在美味的高热量食物面前望而却步，不过一项最新研究有望给他们带来福音。美国研究人员在人体内发现一种负责将碳水化合物转化为脂肪的基因，这一发现有望帮助人们控制体重。
美国加州大学伯克利分校的研究人员发现，一种名为DNA－PK的基因似乎可以控制肝脏将碳水化合物转化为脂肪的过程。在老鼠身上进行的实验表明，当这种基因被破坏后，不论喂给老鼠多少面包、通心粉等高碳水化合物食物，老鼠的体重都不会有明显增加。
研究人员之一罗杰·王说，实验表明，与正常老鼠相比，DNA－PK基因遭到破坏的老鼠更加苗条且体内脂肪要少40％，这主要是因为碳水化合物无法转化成脂肪。
研究人员认为，由于人类也有这一基因，在这一研究基础上未来有望研制出预防肥胖的药物，这样人们就可以放心享用美味的面包、通心粉和米饭等食物，而不用担心身材变胖。
这项研究发表在最新一期《细胞》杂志上。（生物谷Bioon.com）
生物谷推荐原始出处：
Cell,20 March 2009 doi:10.1016/j.cell.2008.12.040
A Role of DNA-PK for the Metabolic Gene Regulation in Response to Insulin
Roger H.F. Wong1,2,Inhwan Chang1,Carolyn S.S. Hudak1,Suzanne Hyun1,Hiu-Yee Kwan1andHei Sook Sul1,2,,
1 Department of Nutritional Science and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA
2 Comparative Biochemistry Program, University of California, Berkeley, Berkeley, CA 94720, USA
Fatty acid synthase (FAS) is a central enzyme in lipogenesis and transcriptionally activated in response to feeding and insulin signaling. The transcription factor USF is required for the activation of FAS transcription, and we show here that USF phosphorylation by DNA-PK, which is dephosphorylated by PP1 in response to feeding, triggers a switch-like mechanism. Under fasting conditions, USF-1 is deacetylated by HDAC9, causing promoter inactivation. In contrast, feeding induces the recruitment of DNA-PK to USF-1 and its phosphorylation, which then allows recruitment of P/CAF, resulting in USF-1 acetylation and FAS promoter activation. DNA break/repair components associated with USF induce transient DNA breaks during FAS activation. In DNA-PK-deficient SCID mice, feeding-induced USF-1 phosphorylation/acetylation, DNA breaks, and FAS activation leading to lipogenesis are impaired, resulting in decreased triglyceride levels. Our study demonstrates that a kinase central to the DNA damage response mediates metabolic gene activation.
