2月10日，日本京都大学等组成的研究团队在美国在线科学杂志PLoS ONE上发表研究成果称，番茄中包含能有效改善代谢综合症的体脂肪燃烧成分。
造成代谢综合症的原因之一是中性脂肪增多导致血脂过高。京大食品功能学教授河田照熊介绍说：“这是首次发现番茄中的成分具有直接燃脂效果。”
该成分与可有效减少中性脂肪的亚油酸属同类物质。虽然番茄被认为对高血脂和糖尿病有效，但此前其具体有效成分并不为人所知。
研究团队在番茄及其果汁中寻找激活燃脂基因的物质，发现了这一新成分。
该团队对肥胖老鼠进行了为期4周的实验。每天在老鼠食用的4g高卡路里饲料中加入0.002克该成分，然后与仅喂养高卡路里饲料的肥胖老鼠进行中性脂肪量和血糖值的测定比较。结果显示，饲料中加入该成分的老鼠血液和肝脏中的中性脂肪减少了约三成，血糖值降低了约两成。有分析认为，这是由于肝脏的糖分吸收能力转好，从而降低了血糖值。（生物谷Bioon.com）
doi:10.1371/journal.pone.0031317
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Potent PPARα Activator Derived from Tomato Juice, 13-oxo-9,11-Octadecadienoic Acid, Decreases Plasma and Hepatic Triglyceride in Obese Diabetic Mice
Young-il Kim, Shizuka Hirai, Tsuyoshi Goto, Chie Ohyane, Haruya Takahashi, Taneaki Tsugane, Chiaki Konishi, Takashi Fujii, Shuji Inai, Yoko Iijima, Koh Aoki, Daisuke Shibata, Nobuyuki Takahashi, Teruo Kawada
Dyslipidemia is a major risk factor for development of several obesity-related diseases. The peroxisome proliferator-activated receptor α (PPARα) is a ligand-activated transcription factor that regulates energy metabolism. Previously, we reported that 9-oxo-10,12-octadecadienoic acid (9-oxo-ODA) is presented in fresh tomato fruits and acts as a PPARα agonist. In addition to 9-oxo-ODA, we developed that 13-oxo-9,11-octadecadienoic acid (13-oxo-ODA), which is an isomer of 9-oxo-ODA, is present only in tomato juice. In this study, we explored the possibility that 13-oxo-ODA acts as a PPARα agonist in vitro and whether its effect ameliorates dyslipidemia and hepatic steatosis in vivo. In vitro luciferase assay experiments revealed that 13-oxo-ODA significantly induced PPARα activation; moreover, the luciferase activity of 13-oxo-ODA was stronger than that of 9-oxo-ODA and conjugated linoleic acid (CLA), which is a precursor of 13-oxo-ODA and is well-known as a potent PPARα activator. In addition to in vitro experiment, treatment with 13-oxo-ODA decreased the levels of plasma and hepatic triglycerides in obese KK-Ay mice fed a high-fat diet. In conclusion, our findings indicate that 13-oxo-ODA act as a potent PPARα agonist, suggesting a possibility to improve obesity-induced dyslipidemia and hepatic steatosis.
